Research progress on the regulatory mechanism of cell senescence in arsenic toxicity: a systematic review.

IF 2.2 4区 医学 Q3 TOXICOLOGY
Toxicology Research Pub Date : 2024-08-22 eCollection Date: 2024-08-01 DOI:10.1093/toxres/tfae136
Yun Gu, Ying Qiu, Yujian Li, Weihua Wen
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引用次数: 0

Abstract

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.

砷中毒细胞衰老调控机制的研究进展:系统综述。
作为一种具有类金属特性的元素,砷普遍存在于环境中,是公认的强致癌物。因此,人类接触砷的问题已成为全球公共卫生部门关注的一个重要问题。大量研究表明,砷通过各种机制诱导细胞衰老,包括引发表观遗传学改变、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。本文整理并总结了细胞衰老参与砷毒性的最新研究进展,并探讨了砷诱导毒性的机制。本研究旨在为今后砷毒性的研究以及预防和治疗策略的开发提供新的视角和方向。
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来源期刊
Toxicology Research
Toxicology Research TOXICOLOGY-
CiteScore
3.60
自引率
0.00%
发文量
82
期刊介绍: A multi-disciplinary journal covering the best research in both fundamental and applied aspects of toxicology
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