Gu Yun, Qiu Ying, Li Yujian, Wen Weihua
The School of Public Health, Dali University, Dali, China.
The Second People's Hospital of Yunnan Province, Kunming, China.
Toxicol Res (Camb). 2024 Aug 22;13(4):tfae136. doi: 10.1093/toxres/tfae136. eCollection 2024 Aug.
As an element with metalloid properties, arsenic is pervasively present in the environment and is recognized as a potent carcinogen. Consequently, the issue of human arsenic exposure has become a significant concern within the global public health sector. Numerous studies have indicated that arsenic induces cellular senescence through various mechanisms, including triggering epigenetic alterations, inducing the senescence-associated secretory phenotype (SASP), promoting telomere shortening, and causing mitochondrial dysfunction. This article collates and summarizes the latest research advancements on the involvement of cellular senescence in arsenic toxicity and explores the mechanisms of arsenic-induced toxicity. This study aims to provide new perspectives and directions for future research on arsenic toxicity and the development of prevention and treatment strategies.
作为一种具有类金属特性的元素，砷广泛存在于环境中，并且被公认为是一种强效致癌物。因此，人类砷暴露问题已成为全球公共卫生领域的重大关注点。众多研究表明，砷通过多种机制诱导细胞衰老，包括引发表观遗传改变、诱导衰老相关分泌表型（SASP）、促进端粒缩短以及导致线粒体功能障碍。本文整理并总结了关于细胞衰老在砷毒性中所起作用的最新研究进展，并探讨了砷诱导毒性的机制。本研究旨在为未来砷毒性研究以及预防和治疗策略的开发提供新的视角和方向。
