Author:
Jain Ashita,Casanova Diego,Padilla Alejandra Valdivia,Paniagua Bojorges Angelica,Kotla Sivareddy,Ko Kyung Ae,Samanthapudi Venkata S. K.,Chau Khanh,Nguyen Minh T. H.,Wen Jake,Hernandez Gonzalez Selina L.,Rodgers Shaefali P.,Olmsted-Davis Elizabeth A.,Hamilton Dale J.,Reyes-Gibby Cielito,Yeung Sai-Ching J.,Cooke John P.,Herrmann Joerg,Chini Eduardo N.,Xu Xiaolei,Yusuf Syed Wamique,Yoshimoto Momoko,Lorenzi Philip L.,Hobbs Brain,Krishnan Sunil,Koutroumpakis Efstratios,Palaskas Nicolas L.,Wang Guangyu,Deswal Anita,Lin Steven H.,Abe Jun-ichi,Le Nhat-Tu
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.
Funder
National Institutes of Health
University of Texas MD Anderson Cancer Center
Subject
Cardiology and Cardiovascular Medicine