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: 31 July 2025 | Viewed by 560

Special Issue Editors


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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

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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

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Keywords

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

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Published Papers (1 paper)

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Research

21 pages, 12541 KiB  
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 (registering DOI) - 28 Apr 2025
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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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