Possible molecular mechanisms underlying the development of atherosclerosis in cancer survivors.
Possible molecular mechanisms underlying the development of atherosclerosis in cancer survivors.
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DOI：
10.3389/fcvm.2023.1186679
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发表时间：
2023
影响因子：
3.6
通讯作者：
Le, Nhat-Tu
中科院分区：
文献类型：
--
作者：
Banerjee, Priyanka;Rosales, Julia Enterria;Chau, Khanh;Nguyen, Minh T. H.;Kotla, Sivareddy;Lin, Steven H.;Deswal, Anita;Dantzer, Robert;Olmsted-Davis, Elizabeth A.;Nguyen, Hung;Wang, Guangyu;Cooke, John P.;Abe, Jun-ichi;Le, Nhat-Tu
接受治疗的癌症幸存者患动脉粥样硬化性心血管疾病（CVD）的风险增加，但其潜在机制尚不清楚。最近的研究表明，化疗可以驱动衰老的癌细胞获得一种称为衰老相关干性（SAS）的增殖表型。这些SAS细胞表现出增强的生长和对癌症治疗的抵抗力，从而促进疾病进展。内皮细胞（EC）衰老与动脉粥样硬化和癌症有关，包括癌症幸存者。癌症治疗方式可诱导EC衰老，导致SAS表型的发展和随后的癌症幸存者动脉粥样硬化。因此，靶向显示SAS表型的衰老ec有望成为治疗该人群动脉粥样硬化性CVD的治疗方法。本综述旨在提供SAS在ECs中的诱导机制及其对癌症幸存者动脉粥样硬化的贡献。我们深入研究了在动脉粥样硬化和癌症中起关键作用的血流紊乱和电离辐射导致EC衰老的机制。包括p90RSK/TERF2IP、TGFβR1/SMAD和BH4信号通路在内的关键信号通路被探索为癌症治疗的潜在靶点。通过了解不同类型的衰老及其相关途径之间的相似性和差异，我们可以为有针对性的干预措施铺平道路，旨在增强这一弱势群体的心血管健康。从本综述中获得的见解可能促进癌症幸存者管理动脉粥样硬化性CVD的新治疗策略的发展。
Cancer survivors undergone treatment face an increased risk of developing atherosclerotic cardiovascular disease (CVD), yet the underlying mechanisms remain elusive. Recent studies have revealed that chemotherapy can drive senescent cancer cells to acquire a proliferative phenotype known as senescence-associated stemness (SAS). These SAS cells exhibit enhanced growth and resistance to cancer treatment, thereby contributing to disease progression. Endothelial cell (EC) senescence has been implicated in atherosclerosis and cancer, including among cancer survivors. Treatment modalities for cancer can induce EC senescence, leading to the development of SAS phenotype and subsequent atherosclerosis in cancer survivors. Consequently, targeting senescent ECs displaying the SAS phenotype hold promise as a therapeutic approach for managing atherosclerotic CVD in this population. This review aims to provide a mechanistic understanding of SAS induction in ECs and its contribution to atherosclerosis among cancer survivors. We delve into the mechanisms underlying EC senescence in response to disturbed flow and ionizing radiation, which play pivotal role in atherosclerosis and cancer. Key pathways, including p90RSK/TERF2IP, TGFβR1/SMAD, and BH4 signaling are explored as potential targets for cancer treatment. By comprehending the similarities and distinctions between different types of senescence and the associated pathways, we can pave the way for targeted interventions aim at enhancing the cardiovascular health of this vulnerable population. The insights gained from this review may facilitate the development of novel therapeutic strategies for managing atherosclerotic CVD in cancer survivors.
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影响因子：
20.1
作者：
Benetos A;Toupance S;Gautier S;Labat C;Kimura M;Rossi PM;Settembre N;Hubert J;Frimat L;Bertrand B;Boufi M;Flecher X;Sadoul N;Eschwege P;Kessler M;Tzanetakou IP;Doulamis IP;Konstantopoulos P;Tzani A;Korou M;Gkogkos A;Perreas K;Menenakos E;Samanidis G;Vasiloglou-Gkanis M;Kark JD;Malikov S;Verhulst S;Aviv A
通讯作者：
Aviv A
影响因子：
4.6
作者：
Kim S;Han JH;Nam DH;Kim GY;Lim JH;Kim JR;Woo CH
通讯作者：
Woo CH
影响因子：
8.7
作者：
Boyle, JJ;Bowyer, DE;Bennett, MR
通讯作者：
Bennett, MR
用于深入分析人肝脏磷酸蛋白质组的酶辅助 RP-RPLC 方法
影响因子：
3.3
作者：
Bian, Yangyang;Song, Chunxia;Zou, Hanfa
通讯作者：
Zou, Hanfa
影响因子：
30.8
作者：
Broccoli, D;Smogorzewska, A;deLange, T
通讯作者：
deLange, T