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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (30 November 2022) | Viewed by 34953

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Special Issue Editors

Dr. Manikandan Panchatcharam

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Guest Editor

LSU Health Sciences Center–Shreveport, Shreveport, LA 71103, USA
Interests: stroke; blood brain barrier; restenosis; oxidative stress; autotaxin; lysolipids
Special Issues, Collections and Topics in MDPI journals

Dr. Sumitra Miriyala

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Guest Editor

LSU Health Sciences Center–Shreveport, Shreveport, LA 71103, USA
Interests: vascular remodeling; stroke; alcohol abuse; myocardial injury; inflammation; lysolipids; drug discovery
Special Issues, Collections and Topics in MDPI journals

Dr. Ara Hosne

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Guest Editor

LSU Health Sciences Center – Shreveport, Shreveport, LA 71103, USA
Interests: chemo vascular remodeling; stroke; alcohol abuse; myocardial injury; inflammation; lysolipids; drug discovery

Special Issue Information

Dear Colleagues,

It is our pleasure to announce the launch of a new Special Issue in the IJMS journal focusing on “Lipid and Cardiovascular Disease”. Despite advancements in the diagnosis and treatment of various stages of disease conditions, cardiovascular disease remains one of the most common leading causes of morbidity and mortality worldwide. Imbalance of the lipid microenvironment crucially contributes to atherosclerosis and is the major risk factor of the underlying cardiovascular disease. Dyslipidemia can lead to the deposition of lipid in the arterial intima, leading to inflammation and vascular remodeling, resulting in atherosclerotic plaque formation. Myocardial infarction and stroke are the lethal consequences of plaque rupture or erosion. Research and review articles on this broad important topic are highly encouraged.

Dr. Manikandan Panchatcharam
Dr. Sumitra Miriyala
Dr. Ara Hosne
Guest Editors

Manuscript Submission Information

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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.

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Keywords

atherosclerosis
myocardial infarction
stroke
inflammation
vascular remodeling
lysolipids
cholesterols

Published Papers (13 papers)

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13 pages, 2248 KiB

Open AccessArticle

Mn(III) Porphyrin, MnTnBuOE-2-PyP⁵⁺, Commonly Known as a Mimic of Superoxide Dismutase Enzyme, Protects Cardiomyocytes from Hypoxia/Reoxygenation Induced Injury via Reducing Oxidative Stress

by Sudha Sharma, Papori Sharma, Utsab Subedi, Susmita Bhattarai, Chloe Miller, Shrivats Manikandan, Ines Batinic-Haberle, Ivan Spasojevic, Hong Sun, Manikandan Panchatcharam and Sumitra Miriyala

Int. J. Mol. Sci. 2023, 24(7), 6159; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24076159 - 24 Mar 2023

Cited by 1 | Viewed by 1383

Abstract

Myocardial ischemia-reperfusion injury (I/R) causes damage to cardiomyocytes through oxidative stress and apoptosis. We investigated the cardioprotective effects of MnTnBuOE-2-PyP⁵⁺ (BMX-001), a superoxide dismutase mimic, in an in vitro model of I/R injury in H9c2 cardiomyocytes. We found that BMX-001 protected against hypoxia/reoxygenation (H/R)-induced oxidative stress, as evident by a significant reduction in intracellular and mitochondrial superoxide levels. BMX-001 pre-treatment also reduced H/R-induced cardiomyocyte apoptosis, as marked by a reduction in TUNEL-positive cells. We further demonstrated that BMX-001 pre-treatment significantly improved mitochondrial function, particularly O₂ consumption, in mouse adult cardiomyocytes subjected to H/R. BMX-001 treatment also attenuated cardiolipin peroxidation, 4-hydroxynonenal (4-HNE) level, and 4-HNE adducted proteins following H/R injury. Finally, the pre-treatment with BMX-001 improved cell viability and lactate dehydrogenase (LDH) activity in H9c2 cells following H/R injury. Our findings suggest that BMX-001 has therapeutic potential as a cardioprotective agent against oxidative stress-induced H/R damage in H9c2 cardiomyocytes. Full article

(This article belongs to the Special Issue Lipids and Cardiovascular Disease)

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18 pages, 6249 KiB

Open AccessArticle

The Autotaxin-LPA Axis Emerges as a Novel Regulator of Smooth Muscle Cell Phenotypic Modulation during Intimal Hyperplasia

by Utsab Subedi, Shrivats Manikandan, Susmita Bhattarai, Papori Sharma, Sudha Sharma, Hong Sun, Sumitra Miriyala and Manikandan Panchatcharam

Int. J. Mol. Sci. 2023, 24(3), 2913; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24032913 - 02 Feb 2023

Cited by 1 | Viewed by 1732

Abstract

Neointimal hyperplasia is characterized by a loss of the contractile phenotype of vascular smooth muscle cells (VSMCs). Our group has recently shown that VSMC proliferation and migration are mediated by lysophosphatidic acid (LPA) during restenosis, but the role of autotaxin (ATX; lysophospholipase D), which produces LPA, remains unclear. Endothelial denudation of the mouse carotid artery was performed to induce neointimal hyperplasia, and the extent of damage caused by the ATX-LPA axis was assessed in VSMCs. We observed the upregulation of ATX activity (p < 0.0002) in the injured carotid artery using an AR2 probe fluorescence assay. Further, the tissue carotid LPA levels were elevated 2.7-fold in carotid vessels, augmenting neointimal hyperplasia. We used an electrical cell–substrate impedance sensor (ECIS) to measure VSMC proliferation and migration. Treatment with an ATX inhibitor (PF8380) or LPA receptor inhibitor (Ki16425) attenuated VSMC proliferation (extracellular signal-regulated kinases) activity and migration in response to recombinant ATX. Indeed, PF8380 treatment rescued the aggravated post-wire injury neointima formation of carotid arteries. The upregulation of ATX following vessel injury leads to LPA production in VSMCs, favoring restenosis. Our observations suggest that inhibition of the ATX-LPA axis could be therapeutically targeted in restenosis to minimize VSMC phenotypic modulation and inflammation after vascular injury. Full article

(This article belongs to the Special Issue Lipids and Cardiovascular Disease)

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14 pages, 4036 KiB

Open AccessArticle

Jatrorrhizine Improves Endothelial Function in Diabetes and Obesity through Suppression of Endoplasmic Reticulum Stress

by Yan Zhou, Yuehan Wang, Chi Teng Vong, Yanyan Zhu, Baojun Xu, Cheng-Chao Ruan, Yitao Wang and Wai San Cheang

Int. J. Mol. Sci. 2022, 23(20), 12064; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232012064 - 11 Oct 2022

Cited by 6 | Viewed by 1629

Abstract

Jatrorrhizine (JAT) is one of the major bioactive protoberberine alkaloids found in rhizoma coptidis, which has hypoglycemic and hypolipidemic potential. This study aimed to evaluate the vasoprotective effects of JAT in diabetes and obesity and the underlying mechanism involved. Mouse aortas, carotid arteries and human umbilical cord vein endothelial cells (HUVECs) were treated with risk factors (high glucose or tunicamycin) with and without JAT ex vivo and in vitro. Furthermore, aortas were obtained from mice with chronic treatment: (1) control; (2) diet-induced obese (DIO) mice fed a high-fat diet (45% kcal% fat) for 15 weeks; and (3) DIO mice orally administered JAT at 50 mg/kg/day for the last 5 weeks. High glucose or endoplasmic reticulum (ER) stress inducer tunicamycin impaired acetylcholine-induced endothelium-dependent relaxations (EDRs) in mouse aortas, induced oxidative stress in carotid arteries and HUVECs, downregulated phosphorylations of Akt at Ser473 and eNOS at Ser1177 and enhanced ER stress in mouse aortas and HUVECs, and these impairments were reversed by cotreatment with JAT. JAT increased NO release in high-glucose-treated mouse aortas and HUVECs. In addition, chronic JAT treatment restored endothelial function with EDRs comparable to the control, increased Akt/eNOS phosphorylation, and attenuated ER stress and oxidative stress in aortas from DIO mice. Blood pressure, glucose sensitivity, fatty liver and its morphological change, as well as plasma levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) and plasma lipid profile, were also normalized by JAT treatment. Collectively, our data may be the first to reveal the vasoprotective effect of JAT that ameliorates endothelial dysfunction in diabetes and obesity through enhancement of the Akt/eNOS pathway and NO bioavailability, as well as suppression of ER stress and oxidative stress. Full article

(This article belongs to the Special Issue Lipids and Cardiovascular Disease)

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17 pages, 3037 KiB

Open AccessArticle

Diet-Induced Hypercholesterolemia Leads to Cardiac Dysfunction and Alterations in the Myocardial Proteome

by Márton Richárd Szabó, Márton Pipicz, Márta Sárközy, Bella Bruszel, Zoltán Szabó and Tamás Csont

Int. J. Mol. Sci. 2022, 23(13), 7387; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23137387 - 02 Jul 2022

Cited by 1 | Viewed by 1549

Abstract

Elevated blood cholesterol is a major risk factor for coronary heart disease. Moreover, direct effects on the myocardium also contribute to the adverse effects of hypercholesterolemia. Here, we investigated the effect of hypercholesterolemia on the cardiac proteome. Male Wistar rats were fed with a laboratory rodent chow supplemented with 2% cholesterol for 8 weeks to induce hypercholesterolemia. The protein expression data obtained from the proteomic characterization of left ventricular samples from normo- and hypercholesterolemic animals were subjected to gene ontology (GO) and protein interaction analyses. Elevated circulating cholesterol levels were accompanied by diastolic dysfunction in cholesterol-fed rats. The proteomic characterization of left ventricular samples revealed altered expression of 45 proteins due to hypercholesterolemia. Based on the Gene Ontology analysis, hypercholesterolemia was associated with disturbed expression of cytoskeletal and contractile proteins. Beta-actin was downregulated in the hypercholesterolemic myocardium, and established a prominent hub of the protein interaction network. Analysis of the unfiltered dataset revealed concordant downregulated expression patterns in proteins associated with the arrangement of the contractile system (e.g., cardiac-specific troponins and myosin complex), and in subunits of the mitochondrial respiratory chain. We conclude that the observed changes in the cardiac proteome may contribute to the development of diastolic dysfunction in hypercholesterolemia. Full article

(This article belongs to the Special Issue Lipids and Cardiovascular Disease)

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15 pages, 4742 KiB

Open AccessArticle

Rotenone-Induced 4-HNE Aggresome Formation and Degradation in HL-1 Cardiomyocytes: Role of Autophagy Flux

by Sudha Sharma, Foram Patel, Hosne Ara, Ezra Bess, Alika Shum, Susmita Bhattarai, Utsab Subedi, Daquonte Sanard Bell, Md. Shenuarin Bhuiyan, Hong Sun, Ines Batinic-Haberle, Manikandan Panchatcharam and Sumitra Miriyala

Int. J. Mol. Sci. 2022, 23(9), 4675; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23094675 - 23 Apr 2022

Cited by 6 | Viewed by 2506

Abstract

Reactive oxygen species (ROS) cause oxidative stress by generating reactive aldehydes known as 4-hydroxynonenal (4-HNE). 4-HNE modifies protein via covalent adduction; however, little is known about the degradation mechanism of 4-HNE-adducted proteins. Autophagy is a dynamic process that maintains cellular homeostasis by removing damaged organelles and proteins. In this study, we determined the role of a superoxide dismutase (SOD) mimetic MnTnBuOE-2-PyP⁵⁺ (MnP, BMX-001) on rotenone-induced 4-HNE aggresome degradation in HL-1 cardiomyocytes. A rotenone treatment (500 nM) given for 24 h demonstrated both increased ROS and 4-HNE aggresome accumulation in HL-1 cardiomyocytes. In addition, cardiomyocytes treated with rotenone displayed an increase in the autophagy marker LC3-II, as shown by immunoblotting and immunofluorescence. A pre-treatment with MnP (20 µM) for 24 h attenuated rotenone-induced ROS formation. An MnP pre-treatment showed decreased 4-HNE aggresomes and LC3-II formation. A rotenone-induced increase in autophagosomes was attenuated by a pre-treatment with MnP, as shown by fluorescent-tagged LC3 (tfLC3). Rotenone increased tubulin hyperacetylation through the ROS-mediated pathway, which was attenuated by MnP. The disruption of autophagy caused HL-1 cell death because a 3-methyladenine inhibitor of autophagosomes caused reduced cell death. Yet, rapamycin, an inducer of autophagy, increased cell death. These results indicated that a pre-treatment with MnP decreased rotenone-induced 4-HNE aggresomes by enhancing the degradation process. Full article

(This article belongs to the Special Issue Lipids and Cardiovascular Disease)

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15 pages, 2897 KiB

Open AccessArticle

The ATX–LPA Axis Regulates Vascular Permeability during Cerebral Ischemic-Reperfusion

by Susmita Bhattarai, Sudha Sharma, Utsab Subedi, Hosne Ara, Alika Shum, Murov Milena, Md. Shenuarin Bhuiyan, Srivatsan Kidambi, Hong Sun, Sumitra Miriyala and Manikandan Panchatcharam

Int. J. Mol. Sci. 2022, 23(8), 4138; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23084138 - 08 Apr 2022

Cited by 9 | Viewed by 2359

Abstract

Endothelial permeability is a major complication that must be addressed during stroke treatment. Study of the mechanisms underlying blood–brain barrier (BBB) disruption and management of the hypoxic stress-induced permeability of the endothelium following reperfusion are both urgently needed for stroke management. Lysophosphatidic acid (LPA), a bioactive lipid essential for basic cellular functions, causes unfavorable outcomes during stroke progression. LPA-producing enzyme autotaxin (ATX) is regulated in ischemic stroke. We used an electrical cell-substrate impedance sensor (ECIS) to measure endothelial permeability. Mitochondrial bioenergetics were obtained using a Seahorse analyzer. AR-2 probe fluorescence assay was used to measure ATX activity. LPA increased endothelial permeability and reduced junctional protein expression in mouse brain microvascular endothelial cells (MBMEC). LPA receptor inhibitors Ki16425 and AM095 attenuated the LPA-induced changes in the endothelial permeability and junctional proteins. LPA significantly diminished mitochondrial function in MBMEC. ATX was upregulated (p < 0.05) in brain microvascular endothelial cells under hypoxic reperfusion. ATX activity and permeability were attenuated with the use of an ATX inhibitor in a mouse stroke model. The upregulation of ATX with hypoxic reperfusion leads to LPA production in brain endothelial cells favoring permeability. Inhibition of the ATX–LPA–LPAR axis could be therapeutically targeted in stroke to achieve better outcomes. Full article

(This article belongs to the Special Issue Lipids and Cardiovascular Disease)

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16 pages, 5360 KiB

Open AccessArticle

Protective Effect of Low-Dose Alcohol Consumption against Post-Ischemic Neuronal Apoptosis: Role of L-PGDS

by Chun Li, Jiyu Li, Ethyn G. Loreno, Sumitra Miriyala, Manikandan Panchatcharam and Hong Sun

Int. J. Mol. Sci. 2022, 23(1), 133; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23010133 - 23 Dec 2021

Cited by 2 | Viewed by 1866

Abstract

Ischemic stroke is one of the leading causes of permanent disability and death in adults worldwide. Apoptosis is a major element contributing to post-ischemic neuronal death. We previously found that low-dose alcohol consumption (LAC) protects against neuronal apoptosis in the peri-infarct cortex following transient focal cerebral ischemia. Lipocalin-type prostaglandin D2 synthase (L-PGDS), which is mainly localized in the central nervous system (CNS), was previously shown to inhibit neuronal apoptosis. Therefore, we determined whether L-PGDS is involved in the protective effect of LAC against post-ischemic neuronal apoptosis. Wild-type (WT), CaMKIIα^CreERT2/+/L-PGDS^+/+, and CaMKIIα^CreERT2/+/L-PGDS^flox/flox mice on a C57BL/6J background were gavage fed with ethanol or volume-matched water once a day for 8 weeks. Tamoxifen (2 mg/day) was given intraperitoneally to CaMKIIα^CreERT2/+/L-PGDS^+/+ and CaMKIIα^CreERT2/+/L-PGDS^flox/flox mice for 5 days during the fourth week. AT-56 (30 mg/kg/day), a selective inhibitor of L-PGDS, was given orally to AT-56-treated WT mice from the fifth week for four weeks. Cerebral ischemia/reperfusion (I/R) injury, TUNEL-positive neurons, and cleaved caspase-3-positive neurons were measured at 24 h of reperfusion after a 90 min unilateral middle cerebral artery occlusion (MCAO). We found that 0.7 g/kg/day but not 2.8 g/kg/day ethanol significantly upregulated L-PGDS in the cerebral cortex. In addition, 0.7 g/kg/day ethanol diminished cerebral ischemia/reperfusion (I/R) injury and TUNEL-positive and cleaved caspase-3-positive neurons in the peri-infarct cortex in WT and CaMKIIα^CreERT2/+/L-PGDS^+/+ mice. Furthermore, the neuroprotective effect of 0.7 g/kg/day ethanol was alleviated in AT-56-treated WT and CaMKIIα^CreERT2/+/L-PGDS^flox/flox mice. Our findings suggest that LAC may protect against cerebral I/R injury by suppressing post-ischemic neuronal apoptosis via an upregulated L-PGDS. Full article

(This article belongs to the Special Issue Lipids and Cardiovascular Disease)

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18 pages, 2581 KiB

Open AccessArticle

The Potential Role of Electronegative High-Density Lipoprotein H5 Subfraction in RA-Related Atherosclerosis

by Ching-Kun Chang, Wei-Chung Cheng, Wen-Lung Ma, Po-Ku Chen, Chu-Huang Chen, Pei-Chun Shen, Chia-Ching Chen, Shih-Hsin Chang, Yi-Hua Lai and Der-Yuan Chen

Int. J. Mol. Sci. 2021, 22(21), 11419; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222111419 - 22 Oct 2021

Cited by 2 | Viewed by 2277

Abstract

Although the heterogeneity of high-density lipoprotein-cholesterol (HDL-c) composition is associated with atherosclerotic cardiovascular risk, the link between electronegative subfractions of HDL-c and atherosclerosis in rheumatoid arthritis (RA) remains unknown. We examined the association of the percentage of the most electronegative subfraction of HDL-c (H5%) and RA-related atherosclerosis. Using anion-exchange purification/fast-protein liquid chromatography, we demonstrated significantly higher H5% in patients (median, 7.2%) than HC (2.8%, p < 0.005). Multivariable regression analysis revealed H5% as a significant predictor for subclinical atherosclerosis. We subsequently explored atherogenic role of H5 using cell-based assay. The results showed significantly higher levels of IL-1β and IL-8 mRNA in H5-treated (mean ± SD, 4.45 ± 1.22 folds, 6.02 ± 1.43-folds, respectively) than H1-treated monocytes (0.89 ± 0.18-folds, 1.03 ± 0.26-folds, respectively, both p < 0.001). In macrophages, H5 upregulated the mRNA and protein expression of IL-1β and IL-8 in a dose-dependent manner, and their expression levels were significantly higher than H1-treated macrophages (all p < 0.001). H5 induced more foam cell formation compared with H1-treated macrophages (p < 0.005). In addition, H5 has significantly lower cholesterol efflux capacity than H1 (p < 0.005). The results of nanoLC-MS/MS approach reveal that the best discriminator between high-H5% and normal-H5% is Apo(a), the main constituent of Lp(a). Moreover, Lp(a) level is a significant predictor for high-H5%. These observations suggest that H5 is involved in RA-related atherosclerosis. Full article

(This article belongs to the Special Issue Lipids and Cardiovascular Disease)

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18 pages, 5608 KiB

Open AccessArticle

Features of Lipid Metabolism in Humanized ApoE Knockin Rat Models

by Yang Wu, Gem Johnson, Fujie Zhao, Yin Wu, Guojun Zhao, Andrew Brown, Shaojin You, Ming-Hui Zou and Ping Song

Int. J. Mol. Sci. 2021, 22(15), 8262; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22158262 - 31 Jul 2021

Cited by 6 | Viewed by 3154

Abstract

Apolipoprotein E (ApoE), an essential plasma apolipoprotein, has three isoforms (E2, E3, and E4) in humans. E2 is associated with type III hyperlipoproteinemia. E4 is the major susceptibility gene to Alzheimer’s disease (AD) and coronary heart disease (CHD). We investigated lipid metabolism and atherosclerotic lesions of novel humanized ApoE knockin (hApoE KI) rats in comparison to wide-type (WT) and ApoE knockout (ApoE KO) rats. The hApoE2 rats showed the lowest bodyweight and white fat mass. hApoE2 rats developed higher serum total cholesterol (TC), total triglyceride (TG), and low- and very low density lipoprotein (LDL-C&VLDL-C). ApoE KO rats also exhibited elevated TC and LDL-C&VLDL-C. Only mild atherosclerotic lesions were detected in hApoE2 and ApoE KO aortic roots. Half of the hApoE2 rats developed hepatic nodular cirrhosis. A short period of the Paigen diet (PD) treatment led to the premature death of the hApoE2 and ApoE KO rats. Severe vascular wall thickening of the coronary and pulmonary arteries was observed in 4-month PD-treated hApoE4 rats. In conclusion, hApoE2 rats develop spontaneous hyperlipidemia and might be suitable for studies of lipid metabolism-related diseases. With the PD challenge, hApoE4 KI rats could be a novel model for the analysis of vascular remodeling. Full article

(This article belongs to the Special Issue Lipids and Cardiovascular Disease)

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Review

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16 pages, 3428 KiB

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A Systematic Review on the Risk Modulators of Myocardial Infarction in the “Young”—Implications of Lipoprotein (a)

by Cristian Stătescu, Larisa Anghel, Laura-Cătălina Benchea, Bogdan-Sorin Tudurachi, Andreea Leonte, Alexandra Zăvoi, Ioana Mădălina Zota, Cristina Prisacariu, Rodica Radu, Ionela-Lăcrămioara Șerban and Radu Andy Sascău

Int. J. Mol. Sci. 2023, 24(6), 5927; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24065927 - 21 Mar 2023

Cited by 3 | Viewed by 1804

Abstract

The presence of a myocardial infarction at a younger age is of special interest, considering the psychological and socioeconomic impact, as well as long-term morbidity and mortality. However, this group has a unique risk profile, with less traditional cardiovascular risk factors that are not well studied. This systematic review aims to evaluate traditional risk factors of myocardial infarction in the “young”, highlighting the clinical implications of lipoprotein (a). We performed a comprehensive search using Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) standards; we systematically searched the PubMed, EMBASE, and Science Direct Scopus databases, using the terms: “myocardial infarction”, “young”, “lipoprotein (a)”, “low-density lipoprotein”, “risk factors”. The search identified 334 articles which were screened, and, at the end, 9 original research articles regarding the implications of lipoprotein (a) in myocardial infarction in the “young” were included in the qualitative synthesis. Elevated lipoprotein (a) levels were independently associated with an increased risk of coronary artery disease, especially in young patients, where this risk increased by threefold. Thus, it is recommended to measure the lipoprotein (a) levels in individuals with suspected familial hypercholesterolaemia or with premature atherosclerotic cardiovascular disease and no other identifiable risk factors, in order to identify patients who might benefit from a more intensive therapeutic approach and follow-up. Full article

(This article belongs to the Special Issue Lipids and Cardiovascular Disease)

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20 pages, 7650 KiB

Open AccessReview

Lipids at the Nexus between Cerebrovascular Disease and Vascular Dementia: The Impact of HDL-Cholesterol and Ceramides

by Domenico Sergi, Enrico Zauli, Veronica Tisato, Paola Secchiero, Giorgio Zauli and Carlo Cervellati

Int. J. Mol. Sci. 2023, 24(5), 4403; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24054403 - 23 Feb 2023

Cited by 8 | Viewed by 2642

Abstract

Cerebrovascular diseases and the subsequent brain hypoperfusion are at the basis of vascular dementia. Dyslipidemia, marked by an increase in circulating levels of triglycerides and LDL-cholesterol and a parallel decrease in HDL-cholesterol, in turn, is pivotal in promoting atherosclerosis which represents a common feature of cardiovascular and cerebrovascular diseases. In this regard, HDL-cholesterol has traditionally been considered as being protective from a cardiovascular and a cerebrovascular prospective. However, emerging evidence suggests that their quality and functionality play a more prominent role than their circulating levels in shaping cardiovascular health and possibly cognitive function. Furthermore, the quality of lipids embedded in circulating lipoproteins represents another key discriminant in modulating cardiovascular disease, with ceramides being proposed as a novel risk factor for atherosclerosis. This review highlights the role of HDL lipoprotein and ceramides in cerebrovascular diseases and the repercussion on vascular dementia. Additionally, the manuscript provides an up-to-date picture of the impact of saturated and omega-3 fatty acids on HDL circulating levels, functionality and ceramide metabolism. Full article

(This article belongs to the Special Issue Lipids and Cardiovascular Disease)

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12 pages, 468 KiB

Open AccessReview

Cholesterol Remnants, Triglyceride-Rich Lipoproteins and Cardiovascular Risk

by Francesco Baratta, Nicholas Cocomello, Mattia Coronati, Domenico Ferro, Daniele Pastori, Francesco Angelico and Maria Del Ben

Int. J. Mol. Sci. 2023, 24(5), 4268; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24054268 - 21 Feb 2023

Cited by 8 | Viewed by 2634

Abstract

Randomized clinical trials with statins and other lipid-lowering drugs have shown the presence of a “residual cardiovascular risk” in those treated to “target” for LDL-cholesterol. This risk is mainly associated to lipid components other than LDL and in particular to remnant cholesterol (RC) and to lipoproteins rich in triglycerides in fasting and non-fasting conditions. During fasting, RCs correspond to the cholesterol content of the VLDL and their partially depleted triglyceride remnant containing apoB-100. Conversely, in non-fasting conditions, RCs include also cholesterol present in chylomicrons containing apoB-48. Therefore, RCs refer to total plasma cholesterol minus HDL-cholesterol and LDL-cholesterol, that is, all the cholesterol present in the VLDL, chylomicrons and in their remnants. A large body of experimental and clinical data suggests a major role of RCs in the development of atherosclerosis. In fact, RCs easily pass the arterial wall and bind to the connective matrix stimulating the progression of smooth muscle cells and the proliferation of resident macrophages. RCs are a causal risk factor for cardiovascular events. Fasting and non-fasting RCs are equivalent for predicting vascular events. Further studies on drugs effect on RC levels and clinical trials to evaluate the efficacy of RC reduction on cardiovascular events are needed. Full article

(This article belongs to the Special Issue Lipids and Cardiovascular Disease)

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19 pages, 1659 KiB

Open AccessReview

Effects of Arachidonic Acid Metabolites on Cardiovascular Health and Disease

by Yan Zhou, Haroon Khan, Jianbo Xiao and Wai San Cheang

Int. J. Mol. Sci. 2021, 22(21), 12029; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222112029 - 06 Nov 2021

Cited by 61 | Viewed by 7240

Abstract

Arachidonic acid (AA) is an essential fatty acid that is released by phospholipids in cell membranes and metabolized by cyclooxygenase (COX), cytochrome P450 (CYP) enzymes, and lipid oxygenase (LOX) pathways to regulate complex cardiovascular function under physiological and pathological conditions. Various AA metabolites include prostaglandins, prostacyclin, thromboxanes, hydroxyeicosatetraenoic acids, leukotrienes, lipoxins, and epoxyeicosatrienoic acids. The AA metabolites play important and differential roles in the modulation of vascular tone, and cardiovascular complications including atherosclerosis, hypertension, and myocardial infarction upon actions to different receptors and vascular beds. This article reviews the roles of AA metabolism in cardiovascular health and disease as well as their potential therapeutic implication. Full article

(This article belongs to the Special Issue Lipids and Cardiovascular Disease)

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