Lactate‐mitochondrial crosstalk: A new direction in the treatment of sepsis‐induced acute kidney injury

IF 3.3 3区 生物学 Q3 CELL BIOLOGY Cell Biology International Pub Date : 2024-09-10 DOI:10.1002/cbin.12240
Zhixiong Wu, Wei Qing Liu, Liang Tang, Qiong Yuan, Yaling Li, Hongyu Hu, Xin Luo, Fan Ouyang
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Abstract

Independent risk factors for sepsis‐associated acute kidney injury (S‐AKI) patients include elevated lactate levels, but the specific mechanism remains unclear. Recently, An et al. discovered that excessive acetylation and inactivation of PDHA1 lead to overproduction of lactate, resulting in mitochondrial fragmentation, ATP depletion, excessive mtROS production, and mitochondrial apoptosis, thereby exacerbating AKI in sepsis. Therefore, understanding the pathophysiological processes of mitochondrial function and lactate generation in SAKI is essential and can aid in the development of novel therapeutic strategies. This review elucidates the pathological mechanisms of mitochondrial autophagy and dynamics in AKI. We also discuss the sources of lactate in SAKI and some consequences of lactonization, which may provide new strategies for improving renal injury and delaying the progression of these diseases.
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乳酸-线粒体串联:治疗败血症所致急性肾损伤的新方向
脓毒症相关急性肾损伤(S-AKI)患者的独立危险因素包括乳酸水平升高,但具体机制仍不清楚。最近,An 等人发现,PDHA1 的过度乙酰化和失活导致乳酸生成过多,导致线粒体破碎、ATP 耗竭、mtROS 生成过多和线粒体凋亡,从而加剧了脓毒症中的 AKI。因此,了解 SAKI 中线粒体功能和乳酸生成的病理生理过程至关重要,有助于开发新的治疗策略。本综述阐明了 AKI 中线粒体自噬和动态的病理机制。我们还讨论了 SAKI 中乳酸的来源以及乳酸化的一些后果,这可能会为改善肾损伤和延缓这些疾病的进展提供新的策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Cell Biology International
Cell Biology International 生物-细胞生物学
CiteScore
7.60
自引率
0.00%
发文量
208
审稿时长
1 months
期刊介绍: Each month, the journal publishes easy-to-assimilate, up-to-the minute reports of experimental findings by researchers using a wide range of the latest techniques. Promoting the aims of cell biologists worldwide, papers reporting on structure and function - especially where they relate to the physiology of the whole cell - are strongly encouraged. Molecular biology is welcome, as long as articles report findings that are seen in the wider context of cell biology. In covering all areas of the cell, the journal is both appealing and accessible to a broad audience. Authors whose papers do not appeal to cell biologists in general because their topic is too specialized (e.g. infectious microbes, protozoology) are recommended to send them to more relevant journals. Papers reporting whole animal studies or work more suited to a medical journal, e.g. histopathological studies or clinical immunology, are unlikely to be accepted, unless they are fully focused on some important cellular aspect. These last remarks extend particularly to papers on cancer. Unless firmly based on some deeper cellular or molecular biological principle, papers that are highly specialized in this field, with limited appeal to cell biologists at large, should be directed towards journals devoted to cancer, there being very many from which to choose.
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