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Cells
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Mechanisms Underlying Cardiovascular Aging
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Mechanisms Underlying Cardiovascular Aging

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 January 2026 | Viewed by 782

Special Issue Editor

Dr. Soheil Saeedi

E-Mail Website
Guest Editor
Center for Translational and Experimental Cardiology (CTEC), Department of Cardiology, University Hospital Zurich, University of Zurich, 8952 Schlieren, Switzerland
Interests: cardiovascular aging; vascular senescence; gut microbiome; redox biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

As we age, our cardiovascular system undergoes significant changes that contribute to cardiovascular diseases, such as atherosclerosis and heart failure. To date, diverse mechanisms have been discovered to underpin these diseases, which potentially lead to aging-associated diseases (AADs). One such example is cellular senescence in various cell types, including endothelial cells and perivascular adipocytes. The senescent cells become pathogenic and taint the neighboring healthy cells through their senescence-messaging secretome (SMS) thus fostering AADs in elderly individuals. Therefore, understanding senescence-promoting mechanisms that promote cardiovascular aging is of paramount importance in order to discover and develop novel senescence-rescue and rejuvenating strategies.

This Special Issue, entitled ‘Mechanisms Underlying Cardiovascular Aging’, will discuss how cellular senescence hallmarks contribute to cardiac‒vascular‒adipose dysfunction and pathologies at both the molecular and clinical levels. It will also highlight the pharmacological senolytic and gene-based rejuvenating therapies that can decelerate and mitigate the deleterious aging processes in the cardiovascular system.

Contributions in the form of original research or reviews are invited.

Dr. Soheil Saeedi
Guest Editor

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 aging
  • cellular senescence
  • epigenetic clock
  • endothelial cells
  • perivascular adipose tissue (PVAT)
  • premature aging
  • senolytics
  • rejuvenating strategies

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Related Special Issue

Published Papers (2 papers)

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Research

21 pages, 6602 KiB  
Article
The Loss of Gonadal Hormones Has a Different Impact on Aging Female and Male Mice Submitted to Heart Failure-Inducing Metabolic Hypertensive Stress
by Diwaba Carmel Teou, Emylie-Ann Labbé, Sara-Ève Thibodeau, Élisabeth Walsh-Wilkinson, Audrey Morin-Grandmont, Ann-Sarah Trudeau, Marie Arsenault and Jacques Couet
Cells 2025, 14(12), 870; https://doi.org/10.3390/cells14120870 - 9 Jun 2025
Abstract
Background: Aging and the female sex are considered risk factors for the development of heart failure with preserved ejection fraction (HFpEF). Unlike other risk factors, such as hypertension, obesity, or diabetes, they do not represent therapeutic targets. Methods: In a recently developed two-hit [...] Read more.
Background: Aging and the female sex are considered risk factors for the development of heart failure with preserved ejection fraction (HFpEF). Unlike other risk factors, such as hypertension, obesity, or diabetes, they do not represent therapeutic targets. Methods: In a recently developed two-hit murine HFpEF model (angiotensin II + high-fat diet; MHS), we studied the relative contributions of the biological sex, aging, and gonadal hormones to cardiac remodeling and function. We aimed to reproduce a frequent HFpEF phenotype in mice characterized by aging, hypertension, the female sex, menopause, and metabolic alterations. Using the MHS mouse model, we studied cardiac remodeling and function in C57Bl6/J mice of both sexes, young (12 weeks) and old (20 months), that were gonadectomized (Gx) or not. Results: We observed that in mice, aging was associated with body weight gain, cardiac hypertrophy (CH), left ventricle (LV) concentric remodeling, and left atrial (LA) enlargement. Diastolic parameters such as E and A wave velocities were modulated by aging but only in females. Submitting young and old mice to MHS for 28 days induced the expected HFpEF phenotype consisting of CH, LV wall thickening, LA enlargement, and diastolic dysfunction with a preserved EF except for old males, in which it was significantly reduced. Young mice were Gx at five weeks, and old mice at six months (over a year before MHS). Gx increased myocardial fibrosis in MHS females and helped preserve the EF in males. Conclusions: Our results suggest that MHS has sex-specific effects on old mice, and the loss of gonadal hormones significantly impacts the observed heart failure phenotype. Full article
(This article belongs to the Special Issue Mechanisms Underlying Cardiovascular Aging)
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18 pages, 2226 KiB  
Article
Short- and Long-Term Endothelial Inflammation Have Distinct Effects and Overlap with Signatures of Cellular Senescence
by Barbora Belakova, José Basílio, Manuel Campos-Medina, Anna F. P. Sommer, Adrianna Gielecińska, Ulrike Resch and Johannes A. Schmid
Cells 2025, 14(11), 806; https://doi.org/10.3390/cells14110806 - 30 May 2025
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Abstract
This study investigates the interplay between cellular senescence and inflammation in human umbilical vein endothelial cells (HUVECs). We employed RNA sequencing to analyze gene expression changes in HUVECs subjected to replicative- or radiation-stress-induced senescence, and we compared these profiles with those of cells [...] Read more.
This study investigates the interplay between cellular senescence and inflammation in human umbilical vein endothelial cells (HUVECs). We employed RNA sequencing to analyze gene expression changes in HUVECs subjected to replicative- or radiation-stress-induced senescence, and we compared these profiles with those of cells under acute or chronic TNFα-mediated inflammation. Our findings reveal that both senescence types exhibited significant upregulation of genes associated with epithelial- (or endothelial) mesenchymal transition (EMT) and inflammatory pathways, indicating a shared molecular response. Notably, chronic inflammation led to a pronounced EMT signature, while acute inflammation primarily activated classical inflammatory responses. Experimental validation confirmed reduced proliferation and increased secretion of pro-inflammatory cytokines (IL-6 and IL-8) in senescent and chronically inflamed cells and substantiated the upregulation of EMT marker genes. Additionally, we observed impaired wound healing capacity in senescent and chronically inflamed cells, highlighting the functional consequences of these cellular states. Our study underscores the critical role of inflammation in exacerbating senescence-related changes, contributing to the understanding of age-related cardiovascular pathologies. These insights may inform future therapeutic strategies aimed at mitigating the effects of aging and inflammation on endothelial function and cardiovascular health. Full article
(This article belongs to the Special Issue Mechanisms Underlying Cardiovascular Aging)
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