Molecular Mechanisms of Aging in Cardiovascular Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 20 June 2024 | Viewed by 1634

Special Issue Editor


E-Mail Website
Guest Editor
Department of Nutrition and Integrative Physiology, Florida State University, Tallahassee, FL 32306, USA
Interests: atherosclerosis; redox biology; berry polyphenols; zinc metabolism; autophagy

Special Issue Information

Dear Colleagues,

Aging is associated with low-grade inflammation that increases predisposition to cardiovascular disease, a leading cause of death worldwide. In older adults, the increase in inflammatory responses promotes atherosclerosis, which results from age-related dysfunction of the endothelium and smooth muscle cells that form blood vessels. Cellular senescence, a hallmark of mammalian aging, is a process in which cells stop proliferating and become dysfunctional. Senescent cells secrete an abnormal variety of molecules, including inflammatory cytokines, reactive oxygen species (ROS), and extracellular matrix components that modify the cellular micro-environment, creating a vicious cycle of inflammation and oxidative stress that causes tissue dysfunction during aging. Senescent vascular cells in vitro present similar changes to the ones observed in aged arteries, such as increased secretion of inflammatory cytokines and ROS in the endothelium and vascular smooth muscle cells (VSMCs) through the senescence-associated secretory phenotype. VSMCs expressing the senescence-associated β-galactosidase, a senescent marker, are found in human plaques, indicating that senescence contributes to vascular dysfunction. The exact triggering mechanisms underlying vascular senescence are incompletely understood.

This Special Issue will focus on molecular mechanisms of aging and atherosclerosis in tissues contributing to cardiovascular function and disease including, but not limited to, the cardiovascular system, liver, gut, adipose tissue, and kidney.

Dr. Gloria Salazar

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

  • senescence
  • atherosclerosis
  • oxidative stress
  • inflammation

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

13 pages, 4441 KiB  
Article
The Duality of Adiponectin: The Role of Sex in Atherosclerosis
by Abigail E. Cullen, Ann M. Centner, Riley Deitado, Vladimir Ukhanov, Judy Muller-Delp and Gloria Salazar
Cells 2024, 13(1), 1; https://doi.org/10.3390/cells13010001 - 19 Dec 2023
Viewed by 1354
Abstract
The hormone adiponectin has many beneficial effects in atherosclerosis, as gene deficiency in adiponectin or its receptor has shown detrimental effects on plaque burden in mice. Our objective was to understand the potential roles adiponectin deficiency has on aortic plaque content, inflammation, and [...] Read more.
The hormone adiponectin has many beneficial effects in atherosclerosis, as gene deficiency in adiponectin or its receptor has shown detrimental effects on plaque burden in mice. Our objective was to understand the potential roles adiponectin deficiency has on aortic plaque content, inflammation, and markers of cardiovascular disease according to sex and age. To study the influence of adiponectin status on sex and atherosclerosis, we used young male and female adipoq−/−apoe−/−, adipoq+/apoe−/−, and apoe−/− mice, which were given a high-fat diet (HFD). Even a 50% reduction in the expression of adiponectin led to a plaque reduction in males and an increase in females compared with apoe−/− controls. Changes in plaque were not attributed to changes in cholesterol or cardiovascular disease markers but correlated with inflammatory markers. Plaque reduction in males was associated with reduced monocyte chemoattractant protein 1 (MCP1) and increased colony stimulating factor 3 (CSF3), while the increase in plaque in females correlated with the opposite effect in these markers. In old mice, both adiponectin-deficient genotypes and sexes accumulated more plaque than their respective apoe−/− controls. The increase in plaque with adiponectin deficiency according to age was not explained by a worsening lipid profile but correlated with increased levels of C-C motif chemokine ligand 5 (CCL5). Overall, our study uncovered genotype-specific effects that differed by sex and age of adiponectin deficiency in atherosclerosis. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Aging in Cardiovascular Disease)
Show Figures

Figure 1

Back to TopTop