Cardiovascular Diseases and Telomeres

Aging is a well-established factor that increases the risk of developing cardiovascular diseases (CVDs), including hypertension, myocardial infarction (MI), stroke, chronic heart failure (HF), atherosclerosis [1], and other numerous pathophysiological conditions, the accumulation of endothelial damage over time, hypertrophy, altered ventricular diastolic function, diminished systolic reverse, and increased arterial stiffness [2]. It is believed that many pathophysiological processes either occur due to cellular or subcellular damage leading to a progressive age-related accumulation of biological “garbage” materials such as lipofuscin, an undegradable lysosomal pigment and aberrant proteins [3], or due to disruption of signaling pathways and modification of chromatin structure. A phenomenon called STASIS: stress or aberrant signaling-induced senescence [4, 5]. STASIS is associated with exposure to increased production of reactive oxygen species (ROS) and reduced extracellular proteolytic activity [6]. However, the primary regulators of STASIS involve the dysfunction of p53, p38MAPK, and cyclin-dependent kinase inhibitors p16INK4a (p16) and p21CIP1 (p21) which prevent the G1 phase of the cell cycle [7, 8]. Several studies have described increased p16INK4a expression in kidneys, myocardium, ventricles, and cardiac arteries [9, 10], thereby senescence-associated cell cycle inhibitor p16INK4a is associated with developing cardiovascular diseases and a decrease in their regenerative capacity [11]. © 2025 Elsevier B.V., All rights reserved.