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 1760
Special Issue Editor
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
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Keywords
- senescence
- atherosclerosis
- oxidative stress
- inflammation
