Sex Differences in Cardiovascular Structure and Function—from Mechanisms to Therapeutics

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 31 May 2026 | Viewed by 1789

Special Issue Editors


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Guest Editor
Department of Pharmaceutical Sciences, Thomas J. Long School of Pharmacy, University of the Pacific, Stockton, CA 95211, USA
Interests: vascular biology; sex differences; metabolic disease

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Guest Editor
1. Biomedical Sciences Program, College of Graduate Studies, Midwestern University, Glendale, AZ 85308, USA
2. College of Medicine Phoenix, University of Arizona, Phoenix, AZ 85004, USA
Interests: vascular biology; aneurysms; endothelial function; angiotensin signaling; genetic aortic diseases
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Special Issue Information

Dear Colleagues,

Sex as a biological variable shapes cardiovascular development, disease risk, clinical presentation, and therapeutic response—yet many pathways and practice patterns remain incompletely understood or underexamined. This Special Issue of Cells invites work that bridges basic discovery with translational and clinical impact, advancing truly sex‐informed cardiovascular research and care.

This Special Issue invites studies that connect cellular and molecular mechanisms (e.g., genomic/epigenomic regulation, mitochondrial and metabolic biology, immune–inflammatory drivers, vascular remodeling, extracellular matrix, and electrophysiology) and hormonal influences (estrogens, androgens, menopause, pregnancy/postpartum) to phenotypes and outcomes across heart and vascular disease. Submissions translating biology into prevention, diagnostics, pharmacologic, and therapeutics are especially encouraged.

Dr. Roshanak Rahimian
Dr. Mitra Esfandiarei
Guest Editors

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Keywords

  • cardiovascular diseases
  • sex hormones
  • sex differences
  • vascular and cell signaling
  • therapeutic targets

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Published Papers (1 paper)

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Research

19 pages, 7200 KB  
Article
Cardiomyocyte Glucocorticoid Receptors Exacerbate Stress Effects in Myocardial Ischemia Injury in Mice
by Analilia Cardenas-Garza, Lilly A. Kamberov, Hemangini A. Dhaibar, Tanja Dudenbostel, Gopi Krishna Kolluru, Christopher G. Kevil, Robert H. Oakley, John A. Cidlowski, Luca Cucullo and Diana Cruz-Topete
Cells 2025, 14(24), 2017; https://doi.org/10.3390/cells14242017 - 18 Dec 2025
Viewed by 1393
Abstract
An increase in mental stress is a recognized risk factor for cardiovascular disease (CVD). The present study investigated the relationships between stress, glucocorticoid receptors (GR), and ischemia/reperfusion (I/R) injury. We subjected male and female mice lacking cardiomyocyte GR (CardioGRKO) and their respective controls [...] Read more.
An increase in mental stress is a recognized risk factor for cardiovascular disease (CVD). The present study investigated the relationships between stress, glucocorticoid receptors (GR), and ischemia/reperfusion (I/R) injury. We subjected male and female mice lacking cardiomyocyte GR (CardioGRKO) and their respective controls to a murine model of mental stress (restraint stress). Following stress exposure, mice from both experimental and control groups underwent I/R injury via surgical ligation of the left anterior descending coronary artery. Our findings suggest that the absence of cardiomyocyte GR mitigates the detrimental effects of restraint stress on infarct size and improves post-I/R survival rates in female mice. We found that cardiomyocyte GR deficiency protects the female heart from stress-induced damage by reducing oxidative stress (superoxide and lipid peroxide production). This study is the first to test the impact of systemic stress on cardiomyocyte GR activation, linking it to redox stress in the heart during I/R injury. Our findings provide proof of concept that stress exacerbates cardiomyocyte GR-mediated responses to myocardial infarction (MI) in the female heart. These insights may contribute to the development of sex-specific treatments and therapies tailored for women. Full article
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