TY - JOUR
T1 - Premature senescence and cardiovascular disease following cancer treatments
T2 - mechanistic insights
AU - Jain, Ashita
AU - Casanova, Diego
AU - Padilla, Alejandra Valdivia
AU - Paniagua Bojorges, Angelica
AU - Kotla, Sivareddy
AU - Ko, Kyung Ae
AU - Samanthapudi, Venkata S.K.
AU - Chau, Khanh
AU - Nguyen, Minh T.H.
AU - Wen, Jake
AU - Hernandez Gonzalez, Selina L.
AU - Rodgers, Shaefali P.
AU - Olmsted-Davis, Elizabeth A.
AU - Hamilton, Dale J.
AU - Reyes-Gibby, Cielito
AU - Yeung, Sai Ching J.
AU - Cooke, John P.
AU - Herrmann, Joerg
AU - Chini, Eduardo N.
AU - Xu, Xiaolei
AU - Yusuf, Syed Wamique
AU - Yoshimoto, Momoko
AU - Lorenzi, Philip L.
AU - Hobbs, Brain
AU - Krishnan, Sunil
AU - Koutroumpakis, Efstratios
AU - Palaskas, Nicolas L.
AU - Wang, Guangyu
AU - Deswal, Anita
AU - Lin, Steven H.
AU - Abe, Jun Ichi
AU - Le, Nhat Tu
N1 - Publisher Copyright:
2023 Jain, Casanova, Padilla, Paniagua Bojorges, Kotla, Ko, Samanthapudi, Chau, Nguyen, Wen, Hernandez Gonzalez, Rodgers, Olmsted-Davis, Hamilton, Reyes-Gibby, Yeung, Cooke, Herrmann, Chini, Xu, Yusuf, Yoshimoto, Lorenzi, Hobbs, Krishnan, Koutroumpakis, Palaskas, Wang, Deswal, Lin, Abe and Le.
PY - 2023
Y1 - 2023
N2 - 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.
AB - 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.
KW - DNA damage
KW - NAD
KW - autophagy
KW - cardio-oncology
KW - fission and fusion
KW - mitochondrial dysfunction
KW - premature senescence
KW - telomere dysfunction
UR - http://www.scopus.com/inward/record.url?scp=85173048833&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85173048833&partnerID=8YFLogxK
U2 - 10.3389/fcvm.2023.1212174
DO - 10.3389/fcvm.2023.1212174
M3 - Review article
AN - SCOPUS:85173048833
SN - 2297-055X
VL - 10
JO - Frontiers in Cardiovascular Medicine
JF - Frontiers in Cardiovascular Medicine
M1 - 1212174
ER -