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Cells
Special Issues
Molecular Pathogenesis of Cardiovascular Diseases
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Molecular Pathogenesis of Cardiovascular Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Cardiovascular System".

Deadline for manuscript submissions: 30 September 2025 | Viewed by 604

Special Issue Editors

Prof. Dr. Guo-Chang Fan

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Guest Editor
Department of Pharmacology and Systems Physiology, University of Cincinnati College of Medicine, Cincinnati, OH 45267-0575, USA
Interests: cardiovascular disease; sepsis; myocardial ischemia–reperfusion injury; inflammation; endothelial cell permeability; macrophages; gene-regulated cell death
Special Issues, Collections and Topics in MDPI journals
Dr. Ao Shi

E-Mail
Guest Editor
Faculty of Medicine, St George’s University of London, London SW17 0RE, UK
Interests: cardiovascular disease; angiogenesis; stem cell; regenerative medicine; extracellular vesicle
Dr. Chen Gao

E-Mail Website
Guest Editor
Department of Pharmacology and Systems Physiology, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
Interests: novel molecular mechanisms for the pathogenesis of cardiac diseases

Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVDs) remain a leading cause of global morbidity and mortality, covering a broad spectrum of conditions such as myocardial infarction, arrhythmias, and atherosclerosis. Understanding the molecular mechanisms driving these diseases is essential for developing targeted and effective therapies.

This Special Issue, "Molecular Pathogenesis of Cardiovascular Diseases", aims to provide the latest insights into the molecular and cellular pathways underlying CVD development and progression. We welcome submissions that investigate the roles of inflammation, fibrosis, immune cell activation, and other key processes in cardiovascular pathology. By integrating diverse perspectives and cutting-edge research, this Special Issue seeks to advance knowledge and inspire novel strategies to combat cardiovascular diseases.

Prof. Dr. Guo-Chang Fan
Dr. Ao Shi
Dr. Chen Gao
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. Cells is an international peer-reviewed open access semimonthly 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 2700 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.

Keywords

  • cardiovascular diseases (CVDs)
  • molecular pathogenesis
  • inflammation
  • fibrosis
  • cell death
  • genetic factors
  • extracellular vesicle
  • environmental factors
  • myocardial infarction
  • atherosclerosis
  • arrhythmia
  • heart failure

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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19 pages, 4954 KiB  
Article
Genetic Predisposition and Mitochondrial Dysfunction in Sudden Cardiac Death: Role of MCU Complex Genetic Variations
by Haoliang Meng, Yan He, Yukun Rui, Mengqi Cai, Dongke Fu, Wanli Bi, Bin Luo and Yuzhen Gao
Cells 2025, 14(10), 728; https://doi.org/10.3390/cells14100728 - 16 May 2025
Viewed by 181
Abstract
Sudden cardiac death (SCD) is a major cause of cardiovascular mortality, with coronary artery disease-related SCD (SCD-CAD) being the most prevalent form. Genetic factors and mitochondrial dysfunction, particularly in calcium homeostasis, are critical in SCD-CAD. However, the specific genetic factors linked to mitochondrial [...] Read more.
Sudden cardiac death (SCD) is a major cause of cardiovascular mortality, with coronary artery disease-related SCD (SCD-CAD) being the most prevalent form. Genetic factors and mitochondrial dysfunction, particularly in calcium homeostasis, are critical in SCD-CAD. However, the specific genetic factors linked to mitochondrial dysfunction in SCD-CAD remain poorly understood. In this case-control study, we analyzed 229 SCD-CAD cases and 598 controls from a Southern Han Chinese population, focusing on 12 insertion-deletion (indel) variants across six mitochondrial calcium uniporter (MCU) complex genes. We used capillary electrophoresis-based multiplex genotyping and performed logistic regression and haplotype analyses to assess the association of these variants with SCD-CAD susceptibility. Four significant indel variants and three risk-associated haplotypes were identified. Two of these indels were previously validated in the GWAS catalog as strongly linked to cardiac disorders. Additionally, Mendelian randomization (MR) analysis revealed a causal relationship between elevated levels of the SMDT1-encoded MCU regulator and increased risks of cardiovascular diseases, including coronary atherosclerosis, myocardial infarction, and cardiomyopathy. These findings highlight the role of MCU complex variants in SCD-CAD susceptibility and suggest their potential as biomarkers for cardiovascular risk stratification. Further research with larger cohorts is needed to confirm these results and explore underlying mechanisms. Full article
(This article belongs to the Special Issue Molecular Pathogenesis of Cardiovascular Diseases)
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Review

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25 pages, 2465 KiB  
Review
Progranulin’s Protective Mechanisms and Therapeutic Potential in Cardiovascular Disease
by Gan Qiao, Yongxiang Lu, Jianping Wu, Chunyang Ren, Roudian Lin and Chunxiang Zhang
Cells 2025, 14(11), 762; https://doi.org/10.3390/cells14110762 - 22 May 2025
Viewed by 236
Abstract
Cardiovascular disease (CVD) remains a leading cause of morbidity and mortality globally, prompting the investigation of novel therapeutic targets. Progranulin (PGRN), a glycoprotein initially associated with neurodegenerative disorders, has emerged as a critical protective agent in cardiovascular health. Recent studies indicate that PGRN [...] Read more.
Cardiovascular disease (CVD) remains a leading cause of morbidity and mortality globally, prompting the investigation of novel therapeutic targets. Progranulin (PGRN), a glycoprotein initially associated with neurodegenerative disorders, has emerged as a critical protective agent in cardiovascular health. Recent studies indicate that PGRN exerts its protective effects through various mechanisms, including the modulation of inflammatory pathways, enhancement of mitochondrial function, and promotion of vascular integrity. By engaging with key signaling pathways, such as PI3K/Akt, NF-κB and Wnt/β-catenin, PGRN mitigates oxidative stress and fosters an environment conducive to cardiac repair following ischemic injury. Furthermore, PGRN’s role in lipid metabolism and vascular smooth muscle cell behavior highlights its complexity in influencing atherogenesis and vascular homeostasis. This review synthesizes current knowledge regarding PGRN’s protective mechanisms in CVD, emphasizing its potential as a therapeutic target and paving the way for innovative approaches to prevent and treat cardiovascular diseases, ultimately improving patient outcomes in this critical area of public health. Full article
(This article belongs to the Special Issue Molecular Pathogenesis of Cardiovascular Diseases)
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