Crosstalk Between Cardiovascular Health and Cellular Metabolism

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (31 May 2026) | Viewed by 912

Special Issue Editors


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Department of Physiology and Immunology, Faculty of Medicine Osijek, University Josip Juraj Strossmayer Osijek, J. Huttlera 4, HR-31000 Osijek, Croatia
Interests: vascular physiology; microcirculation; endothelial function; nutrition; cardiovascular physiology; oxidative stress
Special Issues, Collections and Topics in MDPI journals
Department of Physiology and Immunology, Faculty of Medicine Osijek, University Josip Juraj Strossmayer Osijek, J. Huttlera 4, HR-31000 Osijek, Croatia
Interests: microcirculation; body composition; endothelial function; vascular physiology; nutrition; cardiovascular physiology; arteries; endothelium; salt intake
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular diseases remain a major global health challenge, influenced by a complex interplay between cellular metabolism, oxidative stress, and vascular function. Metabolic pathways regulate energy production, redox balance, and cell signaling processes that are essential for maintaining cardiovascular health. When these systems become dysregulated, they contribute to endothelial dysfunction, inflammation, vascular remodeling, and the progression of cardiovascular diseases.

This Special Issue aims to explore the intricate connections between metabolism, vascular biology, and cardiovascular function across molecular, cellular, and clinical levels. We welcome studies that address oxidative stress, mitochondrial biology, lipid and glucose metabolism, redox signaling, blood rheology, microcirculatory flow, and the role of antioxidants in cardiovascular physiology and pathology. Interdisciplinary contributions spanning biochemistry, pharmacology, translational research, and preventive medicine are highly encouraged.

We warmly invite researchers to submit original research articles, reviews, and short communications that may deepen our understanding of how metabolic and rheological regulation influences cardiovascular health and disease.

We look forward to receiving your valuable contributions.

Sincerely,

Dr. Ivana Jukić
Dr. Ana Stupin
Guest Editors

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Keywords

  • cellular metabolism
  • oxidative stress
  • antioxidants
  • cardiovascular health
  • inflammation
  • metabolic disorders

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Published Papers (1 paper)

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Research

18 pages, 1473 KB  
Article
Disrupted SR–Mitochondria Coupling Drives Ischemia–Reperfusion Vulnerability in the Middle-Aged Rat Heart
by Katarina Leskova Majdova, Maria Bencurova, Maria Kovalska, Peter Kaplan, Peter Racay and Zuzana Tatarkova
Biomedicines 2026, 14(3), 547; https://doi.org/10.3390/biomedicines14030547 - 27 Feb 2026
Cited by 1 | Viewed by 666
Abstract
Background: Myocardial ischemia–reperfusion (IR) injury is associated with dysregulated Ca2+ handling and oxidative stress, particularly in the middle-aged heart. Sarcoplasmic reticulum (SR)–mitochondria communication via mitochondria-associated membranes (MAMs) is essential for coordinating Ca2+ transfer and redox signaling; however, its role in [...] Read more.
Background: Myocardial ischemia–reperfusion (IR) injury is associated with dysregulated Ca2+ handling and oxidative stress, particularly in the middle-aged heart. Sarcoplasmic reticulum (SR)–mitochondria communication via mitochondria-associated membranes (MAMs) is essential for coordinating Ca2+ transfer and redox signaling; however, its role in IR injury in the middle-aged myocardium remains incompletely understood. This study investigated changes in cardiac MAM protein composition and associated functional and oxidative parameters during ischemia and IR. Methods: Middle-aged rat hearts were subjected to global ischemia or IR using the Langendorff perfusion model. Mitochondrial, MAM, and homogenate fractions were analyzed using biochemical, proteomic, and functional assays to assess Ca2+-handling proteins, redox enzymes, lipid peroxidation markers, and mitochondrial antioxidant defenses. Results: Myocardial ischemia and IR disrupted SR–mitochondria communication in middle-aged hearts, leading to impaired Ca2+ handling, redox imbalance, and reduced contractile recovery. Ischemia induced significant MAM remodeling, characterized by reduced mitofusin 2 levels and increased enrichment of voltage-dependent anion channel 1. These changes were associated with disturbed mitochondrial Ca2+ signaling, impaired SR Ca2+ sequestration. Although mitochondrial antioxidant defenses, including MnSOD, were largely preserved, IR was associated with compartment-specific redox alterations within MAMs, as inferred from altered redox enzyme activity and enhanced lipid peroxidation. Conclusions: Disruption of SR–mitochondria coupling and MAM-associated redox regulation represents a key mechanism underlying increased vulnerability to IR injury in the middle-aged heart. Targeting MAM integrity and modulating Ca2+-redox cross-talk may improve cardiac resilience in elderly populations. Full article
(This article belongs to the Special Issue Crosstalk Between Cardiovascular Health and Cellular Metabolism)
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