ATP-induced Cell Death Mechanism

Haoling Zhang, D. Sandai, Zhongwen Zhang, Zhi-Jing Song, Haolong Zhang, Rui Zhao
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Abstract

"ATP-induced cell death" is a novel form of cellular demise identified since 1991, typically characterized by a substantial accumulation of adenosine triphosphate (ATP) and the activation of ATP membrane receptors during the cell death process. The perturbation of ATP homeostasis is intricately linked to mitochondrial function. In recent years, ATP-induced cell death (AICD) has emerged as a discernible pattern of cell demise attributed to heightened levels of extracellular ATP (eATP). This phenomenon is intimately associated with the pathophysiological mechanisms underpinning a plethora of maladies, including malignancies, neurodegenerative disorders, ischemia-reperfusion injury, renal impairment, and hematological conditions. The strategic modulation of ATP-induced cell death to mitigate the onset and progression of these related diseases has garnered significant attention and stands as a focal point in etiological research and therapeutic interventions. Nevertheless, the functional alterations and precise molecular mechanisms governing ATP-induced cell death demand further comprehensive exploration. This paper comprehensively synthesizes the most recent advancements in the understanding of ATP-induced cell death mechanisms, with the overarching objective of serving as a reference for a deeper comprehension of its pathogenesis and the proposition of novel therapeutic targets for the management of associated diseases.
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ATP 诱导的细胞死亡机制
"ATP 诱导的细胞死亡 "是 1991 年以来发现的一种新型细胞死亡形式,其典型特征是细胞死亡过程中三磷酸腺苷(ATP)的大量积累和 ATP 膜受体的激活。三磷酸腺苷平衡紊乱与线粒体功能密切相关。近年来,细胞外 ATP(eATP)水平升高导致的 ATP 诱导细胞死亡(AICD)已成为一种明显的细胞死亡模式。这种现象与恶性肿瘤、神经退行性疾病、缺血再灌注损伤、肾功能损伤和血液病等多种疾病的病理生理机制密切相关。对 ATP 诱导的细胞死亡进行策略性调节,以缓解这些相关疾病的发生和发展,已引起人们的极大关注,并成为病因学研究和治疗干预的焦点。然而,有关 ATP 诱导细胞死亡的功能性改变和精确的分子机制还需要进一步的全面探索。本文全面综述了对 ATP 诱导细胞死亡机制认识的最新进展,其总体目标是为深入理解其发病机制和提出治疗相关疾病的新靶点提供参考。
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