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Atherosclerotic and Cardiometabolic Disease: From Molecular Basis to Therapeutic Advances
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Atherosclerotic and Cardiometabolic Disease: From Molecular Basis to Therapeutic Advances

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 73466

Printed Edition Available!
A printed edition of this Special Issue is available here.

Special Issue Editors

Prof. Dr. Eva Kassi

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Guest Editor
1. Department of Biochemistry, Medical School of Athens, National and Kapodistrian University of Athens, 11527 Athens, Greece
2. Unit of Endocrinology, First Department of Propaedeutic Internal Medicine, Laiko Hospital, National & Kapodistrian University of Athens, 11527 Athens, Greece
Interests: women's health; cardiovascular endocrinology; atherosclerosis; non-alcoholic fatty liver disease; endocrinology of adrenals; oestrogen receptor signalling; glucocorticoid receptor signalling; clock system in benign diseases and malignancies; ICI (immune checkpoint inhibitor)-related endocrinopathies; neuroendocrine tumours; vitamin D; calcium and phosphate metabolic disorders; gynaecological cancers
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Harpal S. Randeva

E-Mail Website
Guest Editor
1. Warwick Medical School, University of Warwick, Coventry CV4 7AL, UK
2. Warwickshire Institute for the Study of Diabetes, Endocrinology and Metabolism (WISDEM), University Hospitals Coventry and Warwickshire NHS Trust, Coventry CV2 2DX, UK
Interests: women's health; endocrinology; gynaecological cancers; PCOS; metabolism; nutrition; diabetes; endocrine-disrupting chemicals (EDCs); links between obesity and cancer
Special Issues, Collections and Topics in MDPI journals
Dr. Ioannis Kyrou

E-Mail Website
Guest Editor
1. Warwick Medical School, University of Warwick, Coventry CV4 7AL, UK
2. Warwickshire Institute for the Study of Diabetes, Endocrinology and Metabolism (WISDEM), University Hospitals Coventry and Warwickshire NHS Trust, Coventry CV2 2DX, UK
3. Centre for Sport, Exercise and Life Sciences, Research Institute for Health & Wellbeing, Coventry University, Coventry CV1 5FB, UK
4. Aston Medical School, College of Health and Life Sciences, Aston University, Birmingham B4 7ET, UK
5. Laboratory of Dietetics and Quality of Life, Department of Food Science and Human Nutrition, School of Food and Nutritional Sciences, Agricultural University of Athens, 11855 Athens, Greece
Interests: metabolism and energy homeostasis; nutrition; cardiovascular endocrinology; cardiovascular disease and atherosclerosis; exercise and health; COVID 19; epidemiology of non-communicable diseases and public health; obesity and obesity-related complications; type 2 diabetes; non-alcoholic fatty liver disease (NAFLD); endocrinology; endocrine-disrupting chemicals; polycystic ovary syndrome (PCOS); mental-health stress and the HPA axis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Over the past decades, important progress has been made in the field of molecular biology of atherogenesis, however, there are still gaps in the knowledge of the underlying pathogenesis.

Moreover, diseases such as non alcoholic fatty liver disease/steatohepatitis, diabetes mellitus, arterial hypertension, dyslipidemia, metabolic syndrome, and chronic kidney disease are tightly connected with atherosclerosis, sharing, at least in part, common molecular pathogenetic mechanisms.

Although cardiovascular diseases (CVDs) still remain the number one cause of death globally, lifestyle modification interventions, as well as pharmacological therapies (anti-hypertensive, lipid-lowering drugs etc.) and advances in cardiovascular surgery have led to the reduction of CVD mortality. This highlights the need for both better prevention strategies and novel targeted anti-atherosclerotic therapies which necessitate detailed studying of the underlying disease mechanisms.

Thereby, we invite colleagues to contribute to the present Special Issue with papers focused on a spectrum of atherosclerosis-related topics, ranging from the molecular and cellular pathways of atherogenesis and atherosclerosis-related diseases to novel pharmacological and molecular targets for treatment of atherosclerosis and related diseases.

Assoc. Prof. Eva Kassi
Prof. Harpal S. Randeva
Assist. Prof. Ioannis Kyrou
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Atherosclerosis
  • coronary artery disease
  • stroke
  • non-alcoholic fatty liver disease
  • diabetes mellitus
  • metabolic syndrome
  • plaque stability
  • endothelial cells
  • vascular inflammation
  • antidiabetic drugs
  • antihypertensive treatments
  • lipid lowering treatments
  • lifestyle interventions
  • molecular targeted therapies

Published Papers (15 papers)

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Editorial

Jump to: Research, Review

6 pages, 221 KiB  
Editorial
Atherosclerotic and Cardio-Metabolic Diseases: From Molecular Basis to Therapeutic Advances
by Eva Kassi, Ioannis Kyrou and Harpal S. Randeva
Int. J. Mol. Sci. 2023, 24(11), 9737; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24119737 - 04 Jun 2023
Cited by 1 | Viewed by 870
Abstract
Cardiovascular diseases (CVDs) still remain the major cause of death worldwide; however, CVD-related mortality has been reduced due to lifestyle modification interventions, as well as novel pharmacological therapies and advances in cardiovascular surgery [...] Full article
(This article belongs to the Special Issue Atherosclerotic and Cardiometabolic Disease: From Molecular Basis to Therapeutic Advances)

Research

Jump to: Editorial, Review

23 pages, 3974 KiB  
Article
Estrogen Receptor Subtypes Elicit a Distinct Gene Expression Profile of Endothelial-Derived Factors Implicated in Atherosclerotic Plaque Vulnerability
by Narjes Nasiri-Ansari, Eliana Spilioti, Ioannis Kyrou, Vassiliki Kalotychou, Antonios Chatzigeorgiou, Despina Sanoudou, Karin Dahlman-Wright, Harpal S. Randeva, Athanasios G. Papavassiliou, Paraskevi Moutsatsou and Eva Kassi
Int. J. Mol. Sci. 2022, 23(18), 10960; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms231810960 - 19 Sep 2022
Cited by 6 | Viewed by 2201
Abstract
In the presence of established atherosclerosis, estrogens are potentially harmful. MMP-2 and MMP-9, their inhibitors (TIMP-2 and TIMP-1), RANK, RANKL, OPG, MCP-1, lysyl oxidase (LOX), PDGF-β, and ADAMTS-4 play critical roles in plaque instability/rupture. We aimed to investigate (i) the effect of estradiol [...] Read more.
In the presence of established atherosclerosis, estrogens are potentially harmful. MMP-2 and MMP-9, their inhibitors (TIMP-2 and TIMP-1), RANK, RANKL, OPG, MCP-1, lysyl oxidase (LOX), PDGF-β, and ADAMTS-4 play critical roles in plaque instability/rupture. We aimed to investigate (i) the effect of estradiol on the expression of the abovementioned molecules in endothelial cells, (ii) which type(s) of estrogen receptors mediate these effects, and (iii) the role of p21 in the estrogen-mediated regulation of the aforementioned factors. Human aortic endothelial cells (HAECs) were cultured with estradiol in the presence or absence of TNF-α. The expression of the aforementioned molecules was assessed by qRT-PCR and ELISA. Zymography was also performed. The experiments were repeated in either ERα- or ERβ-transfected HAECs and after silencing p21. HAECs expressed only the GPR-30 estrogen receptor. Estradiol, at low concentrations, decreased MMP-2 activity by 15-fold, increased LOX expression by 2-fold via GPR-30, and reduced MCP-1 expression by 3.5-fold via ERβ. The overexpression of ERα increased MCP-1 mRNA expression by 2.5-fold. In a low-grade inflammation state, lower concentrations of estradiol induced the mRNA expression of MCP-1 (3.4-fold) and MMP-9 (7.5-fold) and increased the activity of MMP-2 (1.7-fold) via GPR-30. Moreover, p21 silencing resulted in equivocal effects on the expression of the abovementioned molecules. Estradiol induced different effects regarding atherogenic plaque instability through different ERs. The balance of the expression of the various ER subtypes may play an important role in the paradoxical characterization of estrogens as both beneficial and harmful. Full article
(This article belongs to the Special Issue Atherosclerotic and Cardiometabolic Disease: From Molecular Basis to Therapeutic Advances)
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21 pages, 2418 KiB  
Article
Empagliflozin Attenuates Non-Alcoholic Fatty Liver Disease (NAFLD) in High Fat Diet Fed ApoE(-/-) Mice by Activating Autophagy and Reducing ER Stress and Apoptosis
by Narjes Nasiri-Ansari, Chrysa Nikolopoulou, Katerina Papoutsi, Ioannis Kyrou, Christos S. Mantzoros, Georgios Kyriakopoulos, Antonios Chatzigeorgiou, Vassiliki Kalotychou, Manpal S. Randeva, Kamaljit Chatha, Konstantinos Kontzoglou, Gregory Kaltsas, Athanasios G. Papavassiliou, Harpal S. Randeva and Eva Kassi
Int. J. Mol. Sci. 2021, 22(2), 818; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22020818 - 15 Jan 2021
Cited by 152 | Viewed by 14078
Abstract
Aims/hypothesis: SGLT-2 inhibitors (SGLT-2i) have been studied as potential treatments against NAFLD, showing varying beneficial effects. The molecular mechanisms mediating these effects have not been fully clarified. Herein, we investigated the impact of empagliflozin on NAFLD, focusing particularly on ER stress, autophagy and [...] Read more.
Aims/hypothesis: SGLT-2 inhibitors (SGLT-2i) have been studied as potential treatments against NAFLD, showing varying beneficial effects. The molecular mechanisms mediating these effects have not been fully clarified. Herein, we investigated the impact of empagliflozin on NAFLD, focusing particularly on ER stress, autophagy and apoptosis. Methods: Five-week old ApoE(-/-) mice were switched from normal to a high-fat diet (HFD). After five weeks, mice were randomly allocated into a control group (HFD + vehicle) and Empa group (HFD + empagliflozin 10 mg/kg/day) for five weeks. At the end of treatment, histomorphometric analysis was performed in liver, mRNA levels of Fasn, Screbp-1, Scd-1, Ppar-γ, Pck-1, Mcp-1, Tnf-α, Il-6, F4/80, Atf4, Elf2α, Chop, Grp78, Grp94, Χbp1, Ire1α, Atf6, mTor, Lc3b, Beclin-1, P62, Bcl-2 and Bax were measured by qRT-PCR, and protein levels of p-EIF2α, EIF2a, CHOP, LC3II, P62, BECLIN-1 and cleaved CASPASE-8 were assessed by immunoblotting. Results: Empagliflozin-treated mice exhibited reduced fasting glucose, total cholesterol and triglyceride serum levels, as well as decreased NAFLD activity score, decreased expression of lipogenic enzymes (Fasn, Screbp-1c and Pck-1) and inflammatory molecules (Mcp-1 and F4/80), compared to the Control group. Empagliflozin significantly decreased the expression of ER stress molecules Grp78, Ire1α, Xbp1, Elf2α, Atf4, Atf6, Chop, P62(Sqstm1) and Grp94; whilst activating autophagy via increased AMPK phosphorylation, decreased mTOR and increased LC3B expression. Finally, empagliflozin increased the Bcl2/Bax ratio and inhibited CASPASE-8 cleavage, reducing liver cell apoptosis. Immunoblotting analysis confirmed the qPCR results. Conclusion: These novel findings indicate that empagliflozin treatment for five weeks attenuates NAFLD progression in ApoE(-/-) mice by promoting autophagy, reducing ER stress and inhibiting hepatic apoptosis. Full article
(This article belongs to the Special Issue Atherosclerotic and Cardiometabolic Disease: From Molecular Basis to Therapeutic Advances)
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Graphical abstract

11 pages, 779 KiB  
Article
Association of Soluble Suppression of Tumorigenesis-2 (ST2) with Endothelial Function in Patients with Ischemic Heart Failure
by Stathis Dimitropoulos, Vasiliki Chara Mystakidi, Evangelos Oikonomou, Gerasimos Siasos, Vasiliki Tsigkou, Dimitris Athanasiou, Nikolaos Gouliopoulos, Evanthia Bletsa, Aimilios Kalampogias, Georgios Charalambous, Costas Tsioufis, Manolis Vavuranakis and Dimitris Tousoulis
Int. J. Mol. Sci. 2020, 21(24), 9385; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21249385 - 09 Dec 2020
Cited by 15 | Viewed by 2021
Abstract
Soluble suppression of tumorigenesis-2 (sST2) has been introduced as a marker associated with heart failure (HF) pathophysiology and status. Endothelial dysfunction is a component underlying HF pathophysiology. Therefore, we examined the association of arterial wall properties with sST2 levels in patients with HF [...] Read more.
Soluble suppression of tumorigenesis-2 (sST2) has been introduced as a marker associated with heart failure (HF) pathophysiology and status. Endothelial dysfunction is a component underlying HF pathophysiology. Therefore, we examined the association of arterial wall properties with sST2 levels in patients with HF of ischemic etiology. We enrolled 143 patients with stable HF of ischemic etiology and reduced left ventricular ejection fraction (LVEF) and 77 control subjects. Flow-mediated dilation (FMD) was used to evaluate endothelial function and pulse wave velocity (PWV) to assess arterial stiffness. Although there was no significant difference in baseline demographic characteristics, levels of sST2 were increased in HF compared to the control (15.8 (11.0, 21.8) ng/mL vs. 12.5 (10.4, 16.3) ng/mL; p < 0.001). In the HF group, there was a positive correlation of sST2 levels with age (rho = 0.22; p = 0.007) while there was no association of LVEF with sST2 (rho = −0.119; p = 0.17) nor with PWV (rho = 0.1; p = 0.23). Interestingly, sST2 was increased in NYHA III [20.0 (12.3, 25.7) ng/mL] compared to patients with NYHA II (15.0 (10.4, 18.2) ng/mL; p = 0.003) and inversely associated with FMD (rho = −0.44; p < 0.001) even after adjustment for possible confounders. In patients with chronic HF of ischemic etiology, sST2 levels are increased and are associated with functional capacity. There is an inverse association between FMD and sST2 levels, highlighting the interplay between the dysfunctional endothelium and HF pathophysiologic mechanisms. Full article
(This article belongs to the Special Issue Atherosclerotic and Cardiometabolic Disease: From Molecular Basis to Therapeutic Advances)
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18 pages, 8737 KiB  
Article
Dapagliflozin Does Not Modulate Atherosclerosis in Mice with Insulin Resistance
by Alida Taberner-Cortés, Ángela Vinué, Andrea Herrero-Cervera, María Aguilar-Ballester, José Tomás Real, Deborah Jane Burks, Sergio Martínez-Hervás and Herminia González-Navarro
Int. J. Mol. Sci. 2020, 21(23), 9216; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21239216 - 03 Dec 2020
Cited by 4 | Viewed by 2529
Abstract
Type 2 diabetes mellitus (T2DM) increases morbimortality in humans via enhanced susceptibility to cardiovascular disease (CVD). Sodium-glucose co-transporter 2 inhibitors (SGLT2i) are drugs designed for T2DM treatment to diminish hyperglycaemia by reducing up to 90% of renal tube glucose reabsorption. Clinical studies also [...] Read more.
Type 2 diabetes mellitus (T2DM) increases morbimortality in humans via enhanced susceptibility to cardiovascular disease (CVD). Sodium-glucose co-transporter 2 inhibitors (SGLT2i) are drugs designed for T2DM treatment to diminish hyperglycaemia by reducing up to 90% of renal tube glucose reabsorption. Clinical studies also suggest a beneficial action of SGLT2i in heart failure and CVD independent of its hypoglycaemiant effect. In the present study, we explored the effect of SGLT2i dapagliflozin (DAPA) in the metabolism and atherosclerosis in Apoe−/−Irs2+/− mice, which display accelerated atherosclerosis induced by insulin resistance. DAPA treatment of Apoe−/−Irs2+/− mice, which were fed a high-fat, high-cholesterol diet, failed to modify body weight, plasma glucose or lipid. Carbohydrate metabolism characterisation showed no effect of DAPA in the glucose tolerance test (GTT) despite augmented insulin levels during the test. In fact, decreased C-peptide levels in DAPA-treated mice during the GTT suggested impaired insulin release. Consistent with this, DAPA treatment of Apoe−/−Irs2+/− isolated islets displayed lower glucose-stimulated insulin secretion compared with vehicle-treated islets. Moreover, insulin-signalling experiments showed decreased pAKT activation in DAPA-treated adipose tissue indicating impaired insulin signalling in this tissue. No changes were seen in lesion size, vulnerability or content of macrophages, vascular smooth muscle cells, T cells or collagen. DAPA did not affect circulating inflammatory cells or cytokine levels. Hence, this study indicates that DAPA does not protect against atherosclerosis in insulin-resistant mice in hypercholesterolemic conditions. Full article
(This article belongs to the Special Issue Atherosclerotic and Cardiometabolic Disease: From Molecular Basis to Therapeutic Advances)
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18 pages, 4157 KiB  
Article
Circulatory Rejuvenated EPCs Derived from PAOD Patients Treated by CD34+ Cells and Hyperbaric Oxygen Therapy Salvaged the Nude Mouse Limb against Critical Ischemia
by Yin-Chia Chen, Jiunn-Jye Sheu, John Y. Chiang, Pei-Lin Shao, Shun-Cheng Wu, Pei-Hsun Sung, Yi-Chen Li, Yi-Ling Chen, Tien-Hung Huang, Kuan-Hung Chen and Hon-Kan Yip
Int. J. Mol. Sci. 2020, 21(21), 7887; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21217887 - 23 Oct 2020
Cited by 6 | Viewed by 2538
Abstract
This study tested whether circulatory endothelial progenitor cells (EPCs) derived from peripheral arterial occlusive disease (PAOD) patients after receiving combined autologous CD34+ cell and hyperbaric oxygen (HBO) therapy (defined as rejuvenated EPCs) would salvage nude mouse limbs against critical limb ischemia (CLI). Adult-male [...] Read more.
This study tested whether circulatory endothelial progenitor cells (EPCs) derived from peripheral arterial occlusive disease (PAOD) patients after receiving combined autologous CD34+ cell and hyperbaric oxygen (HBO) therapy (defined as rejuvenated EPCs) would salvage nude mouse limbs against critical limb ischemia (CLI). Adult-male nude mice (n = 40) were equally categorized into group 1 (sham-operated control), group 2 (CLI), group 3 (CLI-EPCs (6 × 105) derived from PAOD patient’s circulatory blood prior to CD34+ cell and HBO treatment (EPCPr-T) by intramuscular injection at 3 h after CLI induction) and group 4 (CLI-EPCs (6 × 105) derived from PAOD patient’s circulatory blood after CD34+ cell and HBO treatment (EPCAf-T) by the identical injection method). By 2, 7 and 14 days after the CLI procedure, the ischemic to normal blood flow (INBF) ratio was highest in group 1, lowest in group 2 and significantly lower in group 4 than in group 3 (p < 0.0001). The protein levels of endothelial functional integrity (CD31/von Willebrand factor (vWF)/endothelial nitric-oxide synthase (eNOS)) expressed a similar pattern to that of INBF. In contrast, apoptotic/mitochondrial-damaged (mitochondrial-Bax/caspase-3/PARP/cytosolic-cytochrome-C) biomarkers and fibrosis (Smad3/TGF-ß) exhibited an opposite pattern, whereas the protein expressions of anti-fibrosis (Smad1/5 and BMP-2) and mitochondrial integrity (mitochondrial-cytochrome-C) showed an identical pattern of INBF (all p < 0.0001). The protein expressions of angiogenesis biomarkers (VEGF/SDF-1α/HIF-1α) were progressively increased from groups 1 to 3 (all p < 0.0010). The number of small vessels and endothelial cell surface markers (CD31+/vWF+) in the CLI area displayed an identical pattern of INBF (all p < 0.0001). CLI automatic amputation was higher in group 2 than in other groups (all p < 0.001). In conclusion, EPCs from HBO-C34+ cell therapy significantly restored the blood flow and salvaged the CLI in nude mice. Full article
(This article belongs to the Special Issue Atherosclerotic and Cardiometabolic Disease: From Molecular Basis to Therapeutic Advances)
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Review

Jump to: Editorial, Research

34 pages, 487 KiB  
Review
Genetic and Diet-Induced Animal Models for Non-Alcoholic Fatty Liver Disease (NAFLD) Research
by Christina-Maria Flessa, Narjes Nasiri-Ansari, Ioannis Kyrou, Bianca M. Leca, Maria Lianou, Antonios Chatzigeorgiou, Gregory Kaltsas, Eva Kassi and Harpal S. Randeva
Int. J. Mol. Sci. 2022, 23(24), 15791; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232415791 - 13 Dec 2022
Cited by 17 | Viewed by 5509
Abstract
A rapidly increasing incidence of non-alcoholic fatty liver disease (NAFLD) is noted worldwide due to the adoption of western-type lifestyles and eating habits. This makes the understanding of the molecular mechanisms that drive the pathogenesis of this chronic disease and the development of [...] Read more.
A rapidly increasing incidence of non-alcoholic fatty liver disease (NAFLD) is noted worldwide due to the adoption of western-type lifestyles and eating habits. This makes the understanding of the molecular mechanisms that drive the pathogenesis of this chronic disease and the development of newly approved treatments of utmost necessity. Animal models are indispensable tools for achieving these ends. Although the ideal mouse model for human NAFLD does not exist yet, several models have arisen with the combination of dietary interventions, genetic manipulations and/or administration of chemical substances. Herein, we present the most common mouse models used in the research of NAFLD, either for the whole disease spectrum or for a particular disease stage (e.g., non-alcoholic steatohepatitis). We also discuss the advantages and disadvantages of each model, along with the challenges facing the researchers who aim to develop and use animal models for translational research in NAFLD. Based on these characteristics and the specific study aims/needs, researchers should select the most appropriate model with caution when translating results from animal to human. Full article
(This article belongs to the Special Issue Atherosclerotic and Cardiometabolic Disease: From Molecular Basis to Therapeutic Advances)
14 pages, 801 KiB  
Review
New Progress in Early Diagnosis of Atherosclerosis
by Heyu Meng, Jianjun Ruan, Zhaohan Yan, Yanqiu Chen, Jinsha Liu, Xiangdong Li and Fanbo Meng
Int. J. Mol. Sci. 2022, 23(16), 8939; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23168939 - 11 Aug 2022
Cited by 11 | Viewed by 4108
Abstract
Coronary atherosclerosis is a potentially chronic circulatory condition that endangers human health. The biological cause underpinning cardiovascular disease is coronary atherosclerosis, and acute cardiovascular events can develop due to thrombosis, platelet aggregation, and unstable atherosclerotic plaque rupture. Coronary atherosclerosis is progressive, and three [...] Read more.
Coronary atherosclerosis is a potentially chronic circulatory condition that endangers human health. The biological cause underpinning cardiovascular disease is coronary atherosclerosis, and acute cardiovascular events can develop due to thrombosis, platelet aggregation, and unstable atherosclerotic plaque rupture. Coronary atherosclerosis is progressive, and three specific changes appear, with fat spots and stripes, atherosclerosis and thin-walled fiber atherosclerosis, and then complex changes in arteries. The progression and severity of cardiovascular disease are correlated with various levels of calcium accumulation in the coronary artery. The therapy and diagnosis of coronary atherosclerosis benefit from the initial assessment of the size and degree of calcification. This article will discuss the new progress in the early diagnosis of coronary atherosclerosis in terms of three aspects: imaging, gene and protein markers, and trace elements. This study intends to present the latest methods for diagnosing patients with early atherosclerosis through a literature review. Full article
(This article belongs to the Special Issue Atherosclerotic and Cardiometabolic Disease: From Molecular Basis to Therapeutic Advances)
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11 pages, 4540 KiB  
Review
Coronary Artery Ectasia: Review of the Non-Atherosclerotic Molecular and Pathophysiologic Concepts
by Gavin H. C. Richards, Kathryn L. Hong, Michael Y. Henein, Colm Hanratty and Usama Boles
Int. J. Mol. Sci. 2022, 23(9), 5195; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23095195 - 06 May 2022
Cited by 10 | Viewed by 2184
Abstract
Coronary artery ectasia (CAE) is frequently encountered in clinical practice, conjointly with atherosclerotic CAD (CAD). Given the overlapping cardiovascular risk factors for patients with concomitant CAE and atherosclerotic CAD, a common underlying pathophysiology is often postulated. However, coronary artery ectasia may arise independently, [...] Read more.
Coronary artery ectasia (CAE) is frequently encountered in clinical practice, conjointly with atherosclerotic CAD (CAD). Given the overlapping cardiovascular risk factors for patients with concomitant CAE and atherosclerotic CAD, a common underlying pathophysiology is often postulated. However, coronary artery ectasia may arise independently, as isolated (pure) CAE, thereby raising suspicions of an alternative mechanism. Herein, we review the existing evidence for the pathophysiology of CAE in order to help direct management strategies towards enhanced detection and treatment. Full article
(This article belongs to the Special Issue Atherosclerotic and Cardiometabolic Disease: From Molecular Basis to Therapeutic Advances)
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32 pages, 2866 KiB  
Review
SGLT-2 Inhibitors in NAFLD: Expanding Their Role beyond Diabetes and Cardioprotection
by Theodoros Androutsakos, Narjes Nasiri-Ansari, Athanasios-Dimitrios Bakasis, Ioannis Kyrou, Efstathios Efstathopoulos, Harpal S. Randeva and Eva Kassi
Int. J. Mol. Sci. 2022, 23(6), 3107; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23063107 - 13 Mar 2022
Cited by 51 | Viewed by 7614
Abstract
Non-alcoholic fatty liver disease (NAFLD) is an ‘umbrella’ term, comprising a spectrum ranging from benign, liver steatosis to non-alcoholic steatohepatitis, liver fibrosis and eventually cirrhosis and hepatocellular carcinoma. NAFLD has evolved as a major health problem in recent years. Discovering ways to prevent [...] Read more.
Non-alcoholic fatty liver disease (NAFLD) is an ‘umbrella’ term, comprising a spectrum ranging from benign, liver steatosis to non-alcoholic steatohepatitis, liver fibrosis and eventually cirrhosis and hepatocellular carcinoma. NAFLD has evolved as a major health problem in recent years. Discovering ways to prevent or delay the progression of NAFLD has become a global focus. Lifestyle modifications remain the cornerstone of NAFLD treatment, even though various pharmaceutical interventions are currently under clinical trial. Among them, sodium-glucose co-transporter type-2 inhibitors (SGLT-2i) are emerging as promising agents. Processes regulated by SGLT-2i, such as endoplasmic reticulum (ER) and oxidative stress, low-grade inflammation, autophagy and apoptosis are all implicated in NAFLD pathogenesis. In this review, we summarize the current understanding of the NAFLD pathophysiology, and specifically focus on the potential impact of SGLT-2i in NAFLD development and progression, providing current evidence from in vitro, animal and human studies. Given this evidence, further mechanistic studies would advance our understanding of the exact mechanisms underlying the pathogenesis of NAFLD and the potential beneficial actions of SGLT-2i in the context of NAFLD treatment. Full article
(This article belongs to the Special Issue Atherosclerotic and Cardiometabolic Disease: From Molecular Basis to Therapeutic Advances)
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17 pages, 1191 KiB  
Review
Atrial Fibrillation: Pathogenesis, Predisposing Factors, and Genetics
by Marios Sagris, Emmanouil P. Vardas, Panagiotis Theofilis, Alexios S. Antonopoulos, Evangelos Oikonomou and Dimitris Tousoulis
Int. J. Mol. Sci. 2022, 23(1), 6; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23010006 - 21 Dec 2021
Cited by 92 | Viewed by 11863
Abstract
Atrial fibrillation (AF) is the most frequent arrhythmia managed in clinical practice, and it is linked to an increased risk of death, stroke, and peripheral embolism. The Global Burden of Disease shows that the estimated prevalence of AF is up to 33.5 million [...] Read more.
Atrial fibrillation (AF) is the most frequent arrhythmia managed in clinical practice, and it is linked to an increased risk of death, stroke, and peripheral embolism. The Global Burden of Disease shows that the estimated prevalence of AF is up to 33.5 million patients. So far, successful therapeutic techniques have been implemented, with a high health-care cost burden. As a result, identifying modifiable risk factors for AF and suitable preventive measures may play a significant role in enhancing community health and lowering health-care system expenditures. Several mechanisms, including electrical and structural remodeling of atrial tissue, have been proposed to contribute to the development of AF. This review article discusses the predisposing factors in AF including the different pathogenic mechanisms, sedentary lifestyle, and dietary habits, as well as the potential genetic burden. Full article
(This article belongs to the Special Issue Atherosclerotic and Cardiometabolic Disease: From Molecular Basis to Therapeutic Advances)
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18 pages, 2120 KiB  
Review
Different Approaches in Therapy Aiming to Stabilize an Unstable Atherosclerotic Plaque
by Michal Kowara and Agnieszka Cudnoch-Jedrzejewska
Int. J. Mol. Sci. 2021, 22(9), 4354; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094354 - 21 Apr 2021
Cited by 10 | Viewed by 3881
Abstract
Atherosclerotic plaque vulnerability is a vital clinical problem as vulnerable plaques tend to rupture, which results in atherosclerosis complications—myocardial infarctions and subsequent cardiovascular deaths. Therefore, methods aiming to stabilize such plaques are in great demand. In this brief review, the idea of atherosclerotic [...] Read more.
Atherosclerotic plaque vulnerability is a vital clinical problem as vulnerable plaques tend to rupture, which results in atherosclerosis complications—myocardial infarctions and subsequent cardiovascular deaths. Therefore, methods aiming to stabilize such plaques are in great demand. In this brief review, the idea of atherosclerotic plaque stabilization and five main approaches—towards the regulation of metabolism, macrophages and cellular death, inflammation, reactive oxygen species, and extracellular matrix remodeling have been presented. Moreover, apart from classical approaches (targeted at the general mechanisms of plaque destabilization), there are also alternative approaches targeted either at certain plaques which have just become vulnerable or targeted at the minimization of the consequences of atherosclerotic plaque erosion or rupture. These alternative approaches have also been briefly mentioned in this review. Full article
(This article belongs to the Special Issue Atherosclerotic and Cardiometabolic Disease: From Molecular Basis to Therapeutic Advances)
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12 pages, 6676 KiB  
Review
The Protective Role of Sestrin2 in Atherosclerotic and Cardiac Diseases
by Yoshimi Kishimoto, Kazuo Kondo and Yukihiko Momiyama
Int. J. Mol. Sci. 2021, 22(3), 1200; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22031200 - 26 Jan 2021
Cited by 16 | Viewed by 4043
Abstract
Atherosclerotic disease, such as coronary artery disease (CAD), is known to be a chronic inflammatory disease, as well as an age-related disease. Excessive oxidative stress produced by reactive oxygen species (ROS) contributes to the pathogenesis of atherosclerosis. Sestrin2 is an anti-oxidant protein that [...] Read more.
Atherosclerotic disease, such as coronary artery disease (CAD), is known to be a chronic inflammatory disease, as well as an age-related disease. Excessive oxidative stress produced by reactive oxygen species (ROS) contributes to the pathogenesis of atherosclerosis. Sestrin2 is an anti-oxidant protein that is induced by various stresses such as hypoxia, DNA damage, and oxidative stress. Sestrin2 is also suggested to be associated with aging. Sestrin2 is expressed and secreted mainly by macrophages, endothelial cells, and cardiomyocytes. Sestrin2 plays an important role in suppressing the production and accumulation of ROS, thus protecting cells from oxidative damage. Since sestrin2 is reported to have anti-oxidant and anti-inflammatory properties, it may play a protective role against the progression of atherosclerosis and may be a potential therapeutic target for the amelioration of atherosclerosis. Regarding the association between blood sestrin2 levels and atherosclerotic disease, the blood sestrin2 levels in patients with CAD or carotid atherosclerosis were reported to be high. High blood sestrin2 levels in patients with such atherosclerotic disease may reflect a compensatory response to increased oxidative stress and may help protect against the progression of atherosclerosis. This review describes the protective role of sestrin2 against the progression of atherosclerotic and cardiac diseases. Full article
(This article belongs to the Special Issue Atherosclerotic and Cardiometabolic Disease: From Molecular Basis to Therapeutic Advances)
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27 pages, 4308 KiB  
Review
Therapies for the Treatment of Cardiovascular Disease Associated with Type 2 Diabetes and Dyslipidemia
by María Aguilar-Ballester, Gema Hurtado-Genovés, Alida Taberner-Cortés, Andrea Herrero-Cervera, Sergio Martínez-Hervás and Herminia González-Navarro
Int. J. Mol. Sci. 2021, 22(2), 660; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22020660 - 11 Jan 2021
Cited by 17 | Viewed by 3834
Abstract
Cardiovascular disease (CVD) is the leading cause of death worldwide and is the clinical manifestation of the atherosclerosis. Elevated LDL-cholesterol levels are the first line of therapy but the increasing prevalence in type 2 diabetes mellitus (T2DM) has positioned the cardiometabolic risk as [...] Read more.
Cardiovascular disease (CVD) is the leading cause of death worldwide and is the clinical manifestation of the atherosclerosis. Elevated LDL-cholesterol levels are the first line of therapy but the increasing prevalence in type 2 diabetes mellitus (T2DM) has positioned the cardiometabolic risk as the most relevant parameter for treatment. Therefore, the control of this risk, characterized by dyslipidemia, hypertension, obesity, and insulin resistance, has become a major goal in many experimental and clinical studies in the context of CVD. In the present review, we summarized experimental studies and clinical trials of recent anti-diabetic and lipid-lowering therapies targeted to reduce CVD. Specifically, incretin-based therapies, sodium-glucose co-transporter 2 inhibitors, and proprotein convertase subtilisin kexin 9 inactivating therapies are described. Moreover, the novel molecular mechanisms explaining the CVD protection of the drugs reviewed here indicate major effects on vascular cells, inflammatory cells, and cardiomyocytes, beyond their expected anti-diabetic and lipid-lowering control. The revealed key mechanism is a prevention of acute cardiovascular events by restraining atherosclerosis at early stages, with decreased leukocyte adhesion, recruitment, and foam cell formation, and increased plaque stability and diminished necrotic core in advanced plaques. These emergent cardiometabolic therapies have a promising future to reduce CVD burden. Full article
(This article belongs to the Special Issue Atherosclerotic and Cardiometabolic Disease: From Molecular Basis to Therapeutic Advances)
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18 pages, 1329 KiB  
Review
Unraveling the Role of Epicardial Adipose Tissue in Coronary Artery Disease: Partners in Crime?
by Glória Conceição, Diana Martins, Isabel M. Miranda, Adelino F. Leite-Moreira, Rui Vitorino and Inês Falcão-Pires
Int. J. Mol. Sci. 2020, 21(22), 8866; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21228866 - 23 Nov 2020
Cited by 12 | Viewed by 4542
Abstract
The role of epicardial adipose tissue (EAT) in the pathophysiology of coronary artery disease (CAD) remains unclear. The present systematic review aimed at compiling dysregulated proteins/genes from different studies to dissect the potential role of EAT in CAD pathophysiology. Exhaustive literature research was [...] Read more.
The role of epicardial adipose tissue (EAT) in the pathophysiology of coronary artery disease (CAD) remains unclear. The present systematic review aimed at compiling dysregulated proteins/genes from different studies to dissect the potential role of EAT in CAD pathophysiology. Exhaustive literature research was performed using the keywords “epicardial adipose tissue and coronary artery disease”, to highlight a group of proteins that were consistently regulated among all studies. Reactome, a pathway analysis database, was used to clarify the function of the selected proteins and their intertwined association. SignalP/SecretomeP was used to clarify the endocrine function of the selected proteins. Overall, 1886 proteins/genes were identified from 44 eligible studies. The proteins were separated according to the control used in each study (EAT non-CAD or subcutaneous adipose tissue (SAT) CAD) and by their regulation (up- or downregulated). Using a Venn diagram, we selected the proteins that were upregulated and downregulated (identified as 27 and 19, respectively) in EAT CAD for both comparisons. The analysis of these proteins revealed the main pathways altered in the EAT and how they could communicate with the heart, potentially contributing to CAD development. In summary, in this study, the identified dysregulated proteins highlight the importance of inflammatory processes to modulate the local environment and the progression of CAD, by cellular and metabolic adaptations of epicardial fat that facilitate the formation and progression of atherogenesis of coronaries. Full article
(This article belongs to the Special Issue Atherosclerotic and Cardiometabolic Disease: From Molecular Basis to Therapeutic Advances)
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