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A Focus on Molecular Basis in Cardiac Diseases

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A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Biochemistry, Molecular and Cellular Biology".

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 18711

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Dr. Delia Lidia Şălaru

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Department of Internal Medicine, Faculty of Medicine, Grigore T. Popa University of Medicine and Pharmacy of Iasi, 16 University Street, 700115 Iasi, Romania
Interests: venous and arterial thrombosisme
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Special Issue Information

Dear Colleagues,

Cardiac diseases result from a complex dysfunction of different effectors, pathways, and molecular circuits. Deciphering the underlying mechanisms of heart diseases, integrating known biology with newly discovered advanced molecular technology, opens a new perspective on the possibility of prevention and/or diagnosis of cardiovascular pathology.

In this Special Issue, we invite researchers to submit their findings on novel biomarkers, new pathomechanisms and emerging therapeutic targets from a molecular point of view regarding the entire spectrum of cardiovascular diseases, from atherosclerosis and atherothrombosis to emerging concepts in heart failure. Molecular substrate in arrhythmias, genetic disorders and genetic susceptibility, and highlights on interactions between other organs and systems and structural cardiac diseases are more than welcome.

Dr. Delia Lidia Şălaru
Guest Editor

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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. Current Issues in Molecular Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). 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.

Published Papers (12 papers)

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Research

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19 pages, 35137 KiB

Open AccessArticle

Implications of Activating the ANT2/mTOR/PGC-1α Feedback Loop: Insights into Mitochondria-Mediated Injury in Hypoxic Myocardial Cells

by Meng Zhang, Yuanzhan Yang, Zhu Zhu, Zixuan Chen and Dongyang Huang

Curr. Issues Mol. Biol. 2023, 45(11), 8633-8651; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb45110543 - 27 Oct 2023

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Abstract

Mitochondrial dysfunction is known to play a critical role in the development of cardiomyocyte death during acute myocardial infarction (AMI). However, the exact mechanisms underlying this dysfunction are still under investigation. Adenine nucleotide translocase 2 (ANT2) is a key functional protein in mitochondria. We aimed at exploring the potential benefits of ANT2 inhibition against AMI. We utilized an oxygen–glucose deprivation (OGD) cell model and an AMI mice model to detect cardiomyocyte injury. We observed elevated levels of reactive oxygen species (ROS), disrupted mitochondrial membrane potential (MMP), and increased apoptosis due to the overexpression of ANT2. Additionally, we discovered that ANT2 is involved in myocardial apoptosis by activating the mTOR (mechanistic target of rapamycin kinase)-dependent PGC-1α (PPARG coactivator 1 alpha) pathway, establishing a novel feedback loop during AMI. In our experiments with AC16 cells under OGD conditions, we observed protective effects when transfected with ANT2 siRNA and miR-1203. Importantly, the overexpression of ANT2 counteracted the protective effect resulting from miR-1203 upregulation in OGD-induced AC16 cells. All these results supported that the inhibition of ANT2 could alleviate myocardial cell injury under OGD conditions. Based on these findings, we propose that RNA interference (RNAi) technology, specifically miRNA and siRNA, holds therapeutic potential by activating the ANT2/mTOR/PGC-1α feedback loop. This activation could help mitigate mitochondria-mediated injury in the context of AMI. These insights may contribute to the development of future clinical strategies for AMI. Full article

(This article belongs to the Special Issue A Focus on Molecular Basis in Cardiac Diseases)

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12 pages, 1789 KiB

Open AccessArticle

Hypoxia and HIF-1α Regulate the Activity and Expression of Na,K-ATPase Subunits in H9c2 Cardiomyoblasts

by Beyza Gurler, Gizem Gencay and Emel Baloglu

Curr. Issues Mol. Biol. 2023, 45(10), 8277-8288; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb45100522 - 12 Oct 2023

Viewed by 1497

Abstract

The optimal function of the Na,K-ATPase (NKA) pump is essential for the heart. In ischemic heart disease, NKA activity decreases due to the decreased expression of the pump subunits. Here, we tested whether the hypoxia-inducible transcription factor (HIF-1α), the key signaling molecule regulating the adaptation of cells to hypoxia, is involved in controlling the expression and cellular dynamics of α1- and β1-NKA isoforms and of NKA activity in in-vitro hypoxic H9c2 cardiomyoblasts. HIF-1α was silenced through adenoviral infection, and cells were kept in normoxia (19% O₂) or hypoxia (1% O₂) for 24 h. We investigated the mRNA and protein expression of α1-, β1-NKA using RT-qPCR and Western blot in whole-cell lysates, cell membranes, and cytoplasmic fractions after labeling the cell surface with NHS-SS-biotin and immunoprecipitation. NKA activity and intracellular ATP levels were also measured. We found that in hypoxia, silencing HIF-1α prevented the decreased mRNA expression of α1-NKA but not of β1-NKA. Hypoxia decreased the plasma membrane expression of α1-NKA and β1- NKA compared to normoxic cells. In hypoxic cells, HIF-1α silencing prevented this effect by inhibiting the internalization of α1-NKA. Total protein expression was not affected. The decreased activity of NKA in hypoxic cells was fully prevented by silencing HIF-1α independent of cellular ATP levels. This study is the first to show that in hypoxic H9c2 cardiomyoblasts, HIF-1α controls the internalization and membrane insertion of α1-NKA subunit and of NKA activity. The mechanism behind this regulation needs further investigation. Full article

(This article belongs to the Special Issue A Focus on Molecular Basis in Cardiac Diseases)

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15 pages, 3193 KiB

Open AccessArticle

Targeted Expression to Liver of an antimiR-33 Sponge as a Gene Therapy Strategy against Hypercholesterolemia: In Vitro Study

by Mariela Montaño-Samaniego, Jorge Sánchez-Cedillo, Amellalli Lucas-González, Diana M. Bravo-Estupiñan, Ernesto Alarcón-Hernández, Sandra Rivera-Gutiérrez, José Abraham Balderas-López and Miguel Ibáñez-Hernández

Curr. Issues Mol. Biol. 2023, 45(9), 7043-7057; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb45090445 - 24 Aug 2023

Viewed by 2116

Abstract

Atherosclerosis is the leading cause of cardiovascular diseases in Mexico and worldwide. The membrane transporters ABCA1 and ABCG1 are involved in the reverse transport of cholesterol and stimulate the HDL synthesis in hepatocytes, therefore the deficiency of these transporters promotes the acceleration of atherosclerosis. MicroRNA-33 (miR-33) plays an important role in lipid metabolism and exerts a negative regulation on the transporters ABCA1 and ABCG1. It is known that by inhibiting the function of miR-33 with antisense RNA, HDL levels increase and atherogenic risk decreases. Therefore, in this work, a genetic construct, pPEPCK-antimiR-33-IRES2-EGFP, containing a specific antimiR-33 sponge with two binding sites for miR-33 governed under the PEPCK promoter was designed, constructed, and characterized, the identity of which was confirmed by enzymatic restriction, PCR, and sequencing. Hep G2 and Hek 293 FT cell lines, as well as a mouse hepatocyte primary cell culture were transfected with this plasmid construction showing expression specificity of the PEPCK promoter in hepatic cells. An analysis of the relative expression of miR-33 target messengers showed that the antimiR-33 sponge indirectly induces the expression of its target messengers (ABCA1 and ABCG1). This strategy could open new specific therapeutic options for hypercholesterolemia and atherosclerosis, by blocking the miR-33 specifically in hepatocytes. Full article

(This article belongs to the Special Issue A Focus on Molecular Basis in Cardiac Diseases)

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19 pages, 2355 KiB

Open AccessArticle

Differential Expression of Subsets of Genes Related to HDL Metabolism and Atherogenesis in the Peripheral Blood in Coronary Artery Disease

by Alexander D. Dergunov, Elena V. Nosova, Alexandra V. Rozhkova, Margarita A. Vinogradina, Veronika B. Baserova, Mikhail A. Popov, Svetlana A. Limborska and Liudmila V. Dergunova

Curr. Issues Mol. Biol. 2023, 45(8), 6823-6841; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb45080431 - 16 Aug 2023

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Abstract

Differential expression of genes (DEGs) in coronary artery disease (CAD) and the association between transcript level and high-density lipoprotein cholesterol (HDL-C) were studied with 76 male patients with CAD and 63 control patients. The transcript level of genes related to HDL metabolism (24 genes) and atherosclerosis-prone (41 genes) in RNA isolated from peripheral blood mononuclear cells was measured by real-time RT-PCR. Twenty-eight DEGs were identified. The expression of cholesterol transporters, ALB, APOA1, and LCAT was down-regulated, while the expression of AMN, APOE, LDLR, LPL, PLTP, PRKACA, and CETP was up-regulated. The systemic inflammation in CAD is evidenced by the up-regulation of IL1B, TLR8, CXCL5, and TNFRSF1A. For the controls, TLR8 and SOAT1 were negative predictors of the HDL-C level. For CAD patients, PRKACG, PRKCQ, and SREBF1 were positive predictors, while PRKACB, LCAT, and S100A8 were negative predictors. For CAD patients, the efficiency of reverse cholesterol transport is 73–79%, and intracellular free cholesterol seems to accumulate at hyperalphalipoproteinemia. Both atheroprotective (via S100A8) and proatherogenic (via SREBF1, LCAT, PRKACG, PRKACB, and PRKCQ) associations of gene expression with HDL-C determine HDL functionality in CAD patients. The selected key genes and involved pathways may represent HDL-specific targets for the diagnosis and treatment of CAD and atherosclerosis. Full article

(This article belongs to the Special Issue A Focus on Molecular Basis in Cardiac Diseases)

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11 pages, 965 KiB

Open AccessArticle

Maximal Exercise Improves the Levels of Endothelial Progenitor Cells in Heart Failure Patients

by Suiane Cavalcante, Sofia Viamonte, Rui S. Cadilha, Ilda P. Ribeiro, Ana Cristina Gonçalves, João Sousa-Venâncio, Marisol Gouveia, Manuel Teixeira, Mário Santos, José Oliveira and Fernando Ribeiro

Curr. Issues Mol. Biol. 2023, 45(3), 1950-1960; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb45030125 - 28 Feb 2023

Viewed by 1799

Abstract

The impact of exercise on the levels of endothelial progenitor cells (EPCs), a marker of endothelial repair and angiogenesis, and circulating endothelial cells (CECs), an indicator of endothelial damage, in heart failure patients is largely unknown. This study aims to evaluate the effects of a single exercise bout on the circulating levels of EPCs and CECs in heart failure patients. Thirteen patients with heart failure underwent a symptom-limited maximal cardiopulmonary exercise test to assess exercise capacity. Before and after exercise testing, blood samples were collected to quantify EPCs and CECs by flow cytometry. The circulating levels of both cells were also compared to the resting levels of 13 volunteers (age-matched group). The maximal exercise bout increased the levels of EPCs by 0.5% [95% Confidence Interval, 0.07 to 0.93%], from 4.2 × 10⁻³ ± 1.5 × 10⁻³% to 4.7 × 10⁻³ ± 1.8 × 10⁻³% (p = 0.02). No changes were observed in the levels of CECs. At baseline, HF patients presented reduced levels of EPCs compared to the age-matched group (p = 0.03), but the exercise bout enhanced circulating EPCs to a level comparable to the age-matched group (4.7 × 10⁻³ ± 1.8 × 10⁻³% vs. 5.4 × 10⁻³ ± 1.7 × 10⁻³%, respectively, p = 0.14). An acute bout of exercise improves the potential of endothelial repair and angiogenesis capacity by increasing the circulating levels of EPCs in patients with heart failure. Full article

(This article belongs to the Special Issue A Focus on Molecular Basis in Cardiac Diseases)

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10 pages, 1805 KiB

Open AccessCommunication

Sexual Dimorphism in the Polarization of Cardiac ILCs through Elabela

by Évila Lopes Salles, Sahar Emami Naeini, Bidhan Bhandari, Hesam Khodadadi, Edie Threlkeld, Sholeh Rezaee, William Meeks, Avery Meeks, Aderemi Awe, Ahmed El-Marakby, Jack C. Yu, Lei P. Wang and Babak Baban

Curr. Issues Mol. Biol. 2023, 45(1), 223-232; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb45010017 - 30 Dec 2022

Viewed by 1452

Abstract

Elabela is a component of the apelinergic system and may exert a cardioprotective role by regulating the innate immune responses. Innate lymphoid cells (ILCs) have a significant role in initiating and progressing immune-inflammatory responses. While ILCs have been intensively investigated during the last decade, little is known about their relationship with the apelinergic system and their cardiac diversity in a gender-based paradigm. In this study, we investigated the polarization of cardiac ILCs by Elabela in males versus females in a mouse model. Using flow cytometry and immunohistochemistry analyses, we showed a potential interplay between Elabela and cardiac ILCs and whether such interactions depend on sexual dimorphism. Our findings showed, for the first time, that Elabela is expressed by cardiac ILCs, and its expression is higher in females’ ILC class 3 (ILC3s) compared to males. Females had higher frequencies of ILC1s, and Elabela was able to suppress T-cell activation and the expression of co-stimulatory CD28 in a mixed lymphocyte reaction assay (MLR). In conclusion, our results suggest, for the first time, a protective role for Elabela through its interplay with ILCs and that it can be used as an immunotherapeutic target in the treatment of cardiovascular disorders in a gender-based fashion. Full article

(This article belongs to the Special Issue A Focus on Molecular Basis in Cardiac Diseases)

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18 pages, 690 KiB

Open AccessArticle

Role of Single Nucleotide Polymorphism L55M in the Paraoxonase 1 Gene as a Risk and Prognostic Factor in Acute Coronary Syndrome

by Krastina I. Doneva-Basheva, Konstantin Gospodinov, Tanya Tacheva, Dimo Dimov and Tatyana I. Vlaykova

Curr. Issues Mol. Biol. 2022, 44(12), 5915-5932; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb44120403 - 27 Nov 2022

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Abstract

The aim of the current study is to explore the possible role of L55M, (rs 854560, 163T > A) SNP as a predisposing factor for acute coronary syndrome (ACS) and to assess its potency as a prognostic biomarker for short (1 year) survival and for median (5 years) and 9-year long patients’ outcome. Methods: The current work is a prospective case-control study with 77 patients with acute coronary syndrome (53 with ST-elevation myocardial infarction, STEMI, 14 with non-ST-elevation myocardial infarction, NSTEMI and 10 with unstable angina, UA) and 122 control individuals. Patients were followed-up for 9 years. The genotyping for PON1 L55M SNP was carried on by PCR-RFLP method. Results: The results of the genotyping for PON1 L55M SNP showed a statistically significant difference (p = 0.023) between the controls and the whole group of patients with acute coronary syndrome, as the individuals with genotype with at least one variant M allele had about 2.5-fold higher risk for developing ACS than those which are homozygous of the wild-type L allele (LL genotype). In patients with variant M allele genotypes (LM + MM) which suffer from non-ST-segment elevation ACS (NSTEACS, i.e., UA or NSTEMI), the serum levels of total cholesterol (TC) and triacylglycerols (TAG) are significantly higher than in NSTEACS patients with LL genotype (p = 0.022 for TC and p = 0.015 for TAG). There was no significant difference in the survival rate at the 1st, 5th and 9th year of follow-up between ACS patients with different genotypes, although it is worth to note that in the subgroup of NSTEACS, all patients (n = 13) with variant M allele genotypes (LM + MM) were alive at the end of the first year, while 2 of the patients with LL genotype (18.2%) were dead. Conclusions: The results of our current study suggest that the variant M allele and the M allele genotypes (LM + MM) of the PON1 L55M polymorphism are risk factors for acute coronary syndrome, especially for patients with STEMI, but do not support the possible effect of this polymorphism on the clinical progression and outcome of the patients with ACS either in short or long follow-up periods. Full article

(This article belongs to the Special Issue A Focus on Molecular Basis in Cardiac Diseases)

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11 pages, 1756 KiB

Open AccessArticle

Beneficial Effects of RNS60 in Cardiac Ischemic Injury

by Magdalena A. Zabielska-Kaczorowska, Barbara Wierzbicka, Andreas Kalmes, Ewa M. Slominska, Magdi H. Yacoub and Ryszard T. Smolenski

Curr. Issues Mol. Biol. 2022, 44(10), 4877-4887; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb44100331 - 14 Oct 2022

Cited by 1 | Viewed by 1488

Abstract

RNS60 is a physically modified saline solution hypothesized to contain oxygen nanobubbles. It has been reported to reduce ischemia/reperfusion injury in a pig model of acute myocardial infarction. We investigated the effects of RNS60 during cardiac hypoxia in mice and as an additive to cardioplegic solution in rat hearts. ApoE^−/−LDLr^−/− mice were treated by intravenous injection of RNS60 or saline as a control while monitoring the ECG and post-hypoxic serum release of troponin T and creatine kinase activity. Hearts infused with Custodiol containing 10% RNS60 or saline as the control were subjected to 4 h of 4 °C preservation, followed by an assessment of myocardial metabolites, purine release, and mechanical function. RNS60 attenuated changes in the ECG STU area during hypoxia, while the troponin T concentration and creatine kinase activity were significantly higher in the serum of the controls. During reperfusion after 4 h of cold ischemia, the Custodiol/RNS60-treated hearts had about 30% lower LVEDP and better dp/dt_max and dp/dt_min together with a decreased release of purine catabolites vs. the controls. The myocardial ATP, total adenine nucleotides, and phosphocreatine concentrations were higher in the RNS60-treated hearts. This study indicates that RNS60 enhances cardioprotection in experimental myocardial hypoxia and under conditions of cardioplegic arrest. Improved cardiac energetics are involved in the protective effect, but complete elucidation of the mechanism requires further study. Full article

(This article belongs to the Special Issue A Focus on Molecular Basis in Cardiac Diseases)

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Review

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13 pages, 2102 KiB

Open AccessReview

A Systematic Review of Lipid-Focused Cardiovascular Disease Research: Trends and Opportunities

by Uchenna Alex Anyaegbunam, Piyush More, Jean-Fred Fontaine, Vincent ten Cate, Katrin Bauer, Ute Distler, Elisa Araldi, Laura Bindila, Philipp Wild and Miguel A. Andrade-Navarro

Curr. Issues Mol. Biol. 2023, 45(12), 9904-9916; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb45120618 - 9 Dec 2023

Cited by 1 | Viewed by 1329

Abstract

Lipids are important modifiers of protein function, particularly as parts of lipoproteins, which transport lipophilic substances and mediate cellular uptake of circulating lipids. As such, lipids are of particular interest as blood biological markers for cardiovascular disease (CVD) as well as for conditions linked to CVD such as atherosclerosis, diabetes mellitus, obesity and dietary states. Notably, lipid research is particularly well developed in the context of CVD because of the relevance and multiple causes and risk factors of CVD. The advent of methods for high-throughput screening of biological molecules has recently resulted in the generation of lipidomic profiles that allow monitoring of lipid compositions in biological samples in an untargeted manner. These and other earlier advances in biomedical research have shaped the knowledge we have about lipids in CVD. To evaluate the knowledge acquired on the multiple biological functions of lipids in CVD and the trends in their research, we collected a dataset of references from the PubMed database of biomedical literature focused on plasma lipids and CVD in human and mouse. Using annotations from these records, we were able to categorize significant associations between lipids and particular types of research approaches, distinguish non-biological lipids used as markers, identify differential research between human and mouse models, and detect the increasingly mechanistic nature of the results in this field. Using known associations between lipids and proteins that metabolize or transport them, we constructed a comprehensive lipid–protein network, which we used to highlight proteins strongly connected to lipids found in the CVD-lipid literature. Our approach points to a series of proteins for which lipid-focused research would bring insights into CVD, including Prostaglandin G/H synthase 2 (PTGS2, a.k.a. COX2) and Acylglycerol kinase (AGK). In this review, we summarize our findings, putting them in a historical perspective of the evolution of lipid research in CVD. Full article

(This article belongs to the Special Issue A Focus on Molecular Basis in Cardiac Diseases)

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12 pages, 4621 KiB

Open AccessReview

Heat Shock Proteins (HSPs) and Cardiovascular Complications of Obesity: Searching for Potential Biomarkers

by Yuriy S. Timofeev, Anton R. Kiselev, Olga N. Dzhioeva and Oxana M. Drapkina

Curr. Issues Mol. Biol. 2023, 45(12), 9378-9389; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb45120588 - 23 Nov 2023

Viewed by 1076

Abstract

Heat shock proteins (HSPs), a family of proteins that support cellular proteostasis and perform a protective function under various stress conditions, such as high temperature, intoxication, inflammation, or tissue hypoxia, constitute a promising group of possible biochemical markers for obesity and cardiovascular diseases. HSP27 is involved in essential cellular processes occurring in conditions of obesity and its cardiometabolic complications; it has protective properties, and its secretion may indicate a cellular response to stress. HSP40 plays a controversial role in the pathogenesis of obesity. HSP60 is involved in various pathological processes of the cardiovascular, immune, excretory, and nervous systems and is associated with obesity and concomitant diseases. The hypersecretion of HSP60 is associated with poor prognosis; hence, this protein may become a target for further research on obesity and its cardiovascular complications. According to most studies, intracellular HSP70 is an obesity-promoting factor, whereas extracellular HSP70 exhibited inconsistent dynamics across different patient groups and diagnoses. HSPs are involved in the pathogenesis of cardiovascular pathology. However, in the context of cardiovascular and metabolic pathology, these proteins require further investigation. Full article

(This article belongs to the Special Issue A Focus on Molecular Basis in Cardiac Diseases)

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19 pages, 2095 KiB

Open AccessReview

The Role of the Piezo1 Mechanosensitive Channel in Heart Failure

by Weihua Yuan, Xicheng Zhang and Xiangming Fan

Curr. Issues Mol. Biol. 2023, 45(7), 5830-5848; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb45070369 - 13 Jul 2023

Viewed by 2439

Abstract

Mechanotransduction (MT) is inseparable from the pathobiology of heart failure (HF). However, the effects of mechanical forces on HF remain unclear. This review briefly describes how Piezo1 functions in HF-affected cells, including endothelial cells (ECs), cardiac fibroblasts (CFs), cardiomyocytes (CMs), and immune cells. Piezo1 is a mechanosensitive ion channel that has been extensively studied in recent years. Piezo1 responds to different mechanical forces and converts them into intracellular signals. The pathways that modulate the Piezo1 switch have also been briefly described. Experimental drugs that specifically activate Piezo1-like proteins, such as Yoda1, Jedi1, and Jedi2, are available for clinical studies to treat Piezo1-related diseases. The only mechanosensitive ion-channel-specific inhibitor available is GsMTx4, which can turn off Piezo1 by modulating the local membrane tension. Ultrasound waves can modulate Piezo1 switching in vitro with the assistance of microbubbles. This review provides new possible targets for heart failure therapy by exploring the cellular functions of Piezo1 that are involved in the progression of the disease. Modulation of Piezo1 activity may, therefore, effectively delay the progression of heart failure. Full article

(This article belongs to the Special Issue A Focus on Molecular Basis in Cardiac Diseases)

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15 pages, 822 KiB

Open AccessReview

Advances in Ion Channel, Non-Desmosomal Variants and Autophagic Mechanisms Implicated in Arrhythmogenic Cardiomyopathy

by Kexin Li, Yufeng Jiang, Yiyao Zeng and Yafeng Zhou

Curr. Issues Mol. Biol. 2023, 45(3), 2186-2200; https://0-doi-org.brum.beds.ac.uk/10.3390/cimb45030141 - 7 Mar 2023

Cited by 1 | Viewed by 1359

Abstract

Arrhythmogenic cardiomyopathy (ACM) is a heterogeneous disorder characterized by the replacement of cardiac myocytes with fibro-fatty tissues, leading to abnormal excitation-contraction (EC) coupling and a range of malignant events, such as ventricular tachycardia (VT), sudden cardiac death/arrest (SCD/A) and heart failure (HF). The concept of ACM has recently been ex-tended to include right ventricular cardiomyopathy (ARVC), left ventricular cardiomyopathy (ALVC) and biventricular cardiomyopathy. ARVC is generally seen as the most common type of ACM. The pathogenesis of ACM involves mutation variants in desmosomal or non-desmosomal gene loci, as well as various external factors, such as intense exercise, stress and infections. Ion channel alterations, autophagy and non-desmosomal variants are also important components in the development of ACM. As clinical practice enters the era of precision therapy, it is important to review recent studies on these topics to better diagnose and treat the molecular phase of ACM. Full article

(This article belongs to the Special Issue A Focus on Molecular Basis in Cardiac Diseases)

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