학술논문

Premature senescence and cardiovascular disease following cancer treatments: mechanistic insights
Document Type
article
Source
Frontiers in Cardiovascular Medicine, Vol 10 (2023)
Subject
premature senescence
cardio-oncology
DNA damage
telomere dysfunction
mitochondrial dysfunction
fission and fusion
Diseases of the circulatory (Cardiovascular) system
RC666-701
Language
English
ISSN
2297-055X
Abstract
Cardiovascular disease (CVD) is a leading cause of morbidity and mortality, especially among the aging population. The “response-to-injury” model proposed by Dr. Russell Ross in 1999 emphasizes inflammation as a critical factor in atherosclerosis development, with atherosclerotic plaques forming due to endothelial cell (EC) injury, followed by myeloid cell adhesion and invasion into the blood vessel walls. Recent evidence indicates that cancer and its treatments can lead to long-term complications, including CVD. Cellular senescence, a hallmark of aging, is implicated in CVD pathogenesis, particularly in cancer survivors. However, the precise mechanisms linking premature senescence to CVD in cancer survivors remain poorly understood. This article aims to provide mechanistic insights into this association and propose future directions to better comprehend this complex interplay.