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Cells
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The Cell Biology of Heart Disease
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The Cell Biology of Heart Disease

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 2026 | Viewed by 3784

Special Issue Editors

Dr. Rajeshwary Ghosh

E-Mail Website
Guest Editor
Department of Physiology, University of Tennessee Health Science Center, Translational Science Research Building, 71 S Manassas St., Memphis, TN 38103, USA
Interests: cardiovascular diseases; proteasome; macroautophagy; chaperone-mediated autophagy; heart; aging
Special Issues, Collections and Topics in MDPI journals
Dr. Samreen Sadaf

E-Mail Website
Guest Editor
Pittsburgh Heart, Lung, Blood, and Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, PA 15260, USA
Interests: cardiovascular research; senescence; metabolism and immunology

Special Issue Information

Dear Colleagues,

Cardiovascular diseases (CVDs) are one of the leading causes of death worldwide mostly prevalent in older individuals, but now also common in younger populations due to unhealthy lifestyle, poor diet, lack of physical activity, obesity, stress and diabetes. Our heart is made up of various cell types with distinct functions that contribute to its overall structure and function. Cardiomyocytes are the heart's muscle cells responsible for its contractility. Endothelial cells, responsible for maintaining vascular tone, regulating blood flow and forming a barrier between blood and tissue, form the inner lining of blood vessels in the heart. Cardiac fibroblasts provide structural support to the heart by secreting extracellular matrix proteins, maintaining myocardium integrity, and aiding in wound healing and scar formation. Immune cells, including macrophages, lymphocytes and neutrophils, play crucial roles including inflammation and tissue repair, and are observed in conditions like myocarditis, atherosclerosis and ischemia–reperfusion injury. These different types of cells work together to ensure the proper function of the heart, including its contractility, electrical activity, structural integrity and vascular perfusion. In a disease state, alterations of these cells occur, leading to the development of various CVDs including coronary artery disease (CAD), heart failure, arrhythmias and cardiomyopathies. Understanding the roles and interactions of these cells is crucial for advancing treatments for heart diseases.

In this Special Issue, we create a unique platform where the discussion of the cellular state of in heart during physiological and pathological conditions will be highlighted. Researchers from various CVD backgrounds, including CAD, diabetes and obesity, are invited to contribute their findings.

Dr. Rajeshwary Ghosh
Dr. Samreen Sadaf
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 250 words) can be sent to the Editorial Office for assessment.

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

  • cardiomyopathy
  • endothelial dysfunction
  • cellular senescence
  • fibrosis
  • myocardial infarction
  • inflammation
  • mitochondrial dysfunction
  • CAD
  • arrhythmia
  • heart failure

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Published Papers (4 papers)

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Research

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25 pages, 50583 KB  
Article
Epicardial Abnormalities and Mesenchymal/Hematopoietic Cell Expansion in Plakophilin 2-Null Mouse Embryonic Hearts
by Mistura Dolapo Bolaji, Pia E. Hartmann, Eva Miriam Buhl, Robin M. W. Colpaert, Francesca Gasparella, Leon J. de Windt, Martina Calore, Rudolf E. Leube and Hoda Moazzen
Cells 2025, 14(22), 1751; https://doi.org/10.3390/cells14221751 - 8 Nov 2025
Cited by 1 | Viewed by 1216
Abstract
Desmosomal junctions provide structural stability supporting concerted cardiomyocyte contractility. Previously, we demonstrated that a deficiency in the desmosomal transmembrane cadherin desmoglein 2 (Dsg2) reduces desmosome formation and disrupts cardiac morphogenesis, leading to excessive endothelial-to-hematopoietic cell transformation and embryonic lethality. It remained unclear whether [...] Read more.
Desmosomal junctions provide structural stability supporting concerted cardiomyocyte contractility. Previously, we demonstrated that a deficiency in the desmosomal transmembrane cadherin desmoglein 2 (Dsg2) reduces desmosome formation and disrupts cardiac morphogenesis, leading to excessive endothelial-to-hematopoietic cell transformation and embryonic lethality. It remained unclear whether this phenotype was specifically driven by Dsg2-deficiency or was a broader consequence of impaired desmosome adhesion. To address this question, we generated Pkp2mt/mt mouse embryos lacking the desmosomal plaque protein Pkp2, which resulted in loss of desmosome formation. Despite the absence of cardiac wall rupture, Pkp2mt/mt and some Pkp2wt/mt presented accumulations of Ter-119+ blood cells and RUNX1+/CD44+ hematopoietic stem cells in the pericardial space. Remarkably, in Pkp2mt/mt hearts, the epicardium was detached from the myocardium, contained rounded cells expressing the hematopoietic stem cell marker RUNX1, and showed altered intermediate filament expression. These findings suggest a potential trans-differentiation of the epicardial cells into hematopoietic cells. In conclusion, deficiencies in both Dsg2 and Pkp2 promote hematopoiesis in the developing murine heart but target different cell types, i.e., endothelial cells, which lack desmosomes, or desmosome-containing epicardial cells. Our results provide evidence for the involvement of Pkp2 in epicardial morphogenesis and remodeling. Full article
(This article belongs to the Special Issue The Cell Biology of Heart Disease)
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21 pages, 12541 KB  
Article
ATIP1 Is a Suppressor of Cardiac Hypertrophy and Modulates AT2-Dependent Signaling in Cardiac Myocytes
by Tobias Fischer, Sina Gredy, Nadine Scheel, Peter M. Benz, Benjamin Fissler, Melanie Ullrich, Marco Abeßer, Adam G. Rokita, Jochen Reichle, Lars S. Maier, Oliver Ritter, Hideo A. Baba and Kai Schuh
Cells 2025, 14(9), 645; https://doi.org/10.3390/cells14090645 - 28 Apr 2025
Viewed by 1034
Abstract
So far, the molecular functions of the angiotensin-type-2 receptor (AT2) interacting protein (ATIP1) have remained unclear, although expression studies have revealed high levels of ATIP1 in the heart. To unravel its physiological function, we investigated ATIP1-KO mice. They develop a spontaneous cardiac hypertrophy [...] Read more.
So far, the molecular functions of the angiotensin-type-2 receptor (AT2) interacting protein (ATIP1) have remained unclear, although expression studies have revealed high levels of ATIP1 in the heart. To unravel its physiological function, we investigated ATIP1-KO mice. They develop a spontaneous cardiac hypertrophy with a significantly increased heart/bodyweight ratio, enlarged cardiomyocyte diameters, and augmented myocardial fibrosis. Hemodynamic measurements revealed an increased ejection fraction (EF) in untreated ATIP1-KO mice, and reduced end-systolic and end-diastolic volumes (ESV and EDV), which, in sum, reflect a compensated concentric cardiac hypertrophy. Importantly, no significant differences in blood pressure (BP) were observed. Chronic angiotensin II (AngII) infusion resulted in increases in BP and EF in ATIP1-KO and WT mice. Reductions in ESV and EDV occurred in both ATIP1-KO and WT but to a lesser extent in ATIP1-KOs. Isolated cardiomyocytes exhibited a significantly increased contractility in ATIP1-KO and accelerated Ca2+ decay. AngII treatment resulted in increased fractional shortening in WT but decreased shortening in ATIP1-KO, accompanied by accelerated cell relaxation in WT but absent effects on relaxation in ATIP1-KO cells. The AT2 agonist CGP42112A increased shortening in WT cardiomyocytes but, again, did not affect shortening in ATIP1-KO cells. Relaxation was accelerated by CGP42112A in WT but was unaffected in ATIP1-KO cells. We show that ATIP1 deficiency results in spontaneous cardiac hypertrophy in vivo and that ATIP1 is a downstream signal in the AT2 pathway regulating cell contractility. We hypothesize that the latter effect is because of a disinhibition of the AT1 pathway by impaired AT2 signaling. Full article
(This article belongs to the Special Issue The Cell Biology of Heart Disease)
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Review

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25 pages, 652 KB  
Review
Ceramides in the Heart: Physiological and Pathological Roles and Regulation
by Xinyi Chen, Oveena Fonseka, Yihua Han and Wei Liu
Cells 2026, 15(9), 780; https://doi.org/10.3390/cells15090780 (registering DOI) - 25 Apr 2026
Abstract
Ceramides are central bioactive sphingolipids that regulate diverse cellular processes, including membrane organization, energy metabolism, and stress signaling. Emerging evidence has implicated that ceramide dysregulation is associated with the onset and progression of heart failure. This review introduces the understanding of ceramide metabolism, [...] Read more.
Ceramides are central bioactive sphingolipids that regulate diverse cellular processes, including membrane organization, energy metabolism, and stress signaling. Emerging evidence has implicated that ceramide dysregulation is associated with the onset and progression of heart failure. This review introduces the understanding of ceramide metabolism, focusing on its biosynthesis, and functional roles in cardiomyocytes. In addition, the contribution of systemic ceramides derived from circulating lipoproteins and peripheral tissues to cardiovascular risk is also discussed. In parallel, it is highlighted that cardiomyocyte-intrinsic ceramide synthesis plays physiological and pathological roles in the heart. Particularly, excessive ceramide accumulation is detrimental for cardiac function, through multiple mechanisms, such as lipotoxic effects, mitochondrial impairment, inflammation, and cell death. The current review discusses the potential diagnostic and therapeutic strategies targeting ceramide metabolism, as well as the open questions about ceramide association with heart disease. Full article
(This article belongs to the Special Issue The Cell Biology of Heart Disease)
19 pages, 1886 KB  
Review
Per- and Polyfluoroalkyl Substances (PFAS) Within the Exposome: Cellular and Molecular Mechanisms Underlying a Potential Risk for Cardiac Arrhythmias and Atrial Fibrillation?
by Mikaelys Plantier, Nour Naji, Andréane Dupont and Roddy Hiram
Cells 2026, 15(8), 696; https://doi.org/10.3390/cells15080696 - 15 Apr 2026
Viewed by 336
Abstract
Background: Per- and polyfluoroalkyl substances (PFAS) represent a large class of synthetic fluorinated compounds characterized by highly stable carbon–fluorine bonds that confer exceptional environmental persistence and bioaccumulative properties. Although regulatory measures have restricted the production of several PFAS, including perfluorooctanoic acid (PFOA) [...] Read more.
Background: Per- and polyfluoroalkyl substances (PFAS) represent a large class of synthetic fluorinated compounds characterized by highly stable carbon–fluorine bonds that confer exceptional environmental persistence and bioaccumulative properties. Although regulatory measures have restricted the production of several PFAS, including perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS), their environmental persistence continues to maintain widespread human exposure, while newly introduced replacement compounds raise additional toxicological concerns. Notably, the recent evidence demonstrating PFAS-induced alterations in key cardiac ion channel activity and electrocardiographic parameters suggest potential electrophysiological mechanisms that may contribute to arrhythmogenesis and cardiac arrhythmias including the most frequent one, atrial fibrillation (AF). Methods: We conducted a narrative literature review of experimental, epidemiological, and mechanistic studies investigating and reporting the cardiovascular, electrophysiological, and potential arrhythmogenic effects of PFAS. Results: Available evidence indicates that PFAS exposure is associated with alterations in cardiac electrophysiology, including modulation of ion channel activity (notably sodium, calcium, and potassium channels), disruption of calcium handling, and changes in electrocardiographic parameters such as QT interval prolongation, which are key contributors to arrhythmogenesis and AF. Conclusions: This review highlights the need for improved understanding of PFAS-induced electrophysiological alterations, to clarify the role of PFAS in cardiac arrhythmias including AF. Full article
(This article belongs to the Special Issue The Cell Biology of Heart Disease)
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