Role of Mitochondrial Therapy for Ischemic-Reperfusion Injury and Acute Kidney Injury.
Role of Mitochondrial Therapy for Ischemic-Reperfusion Injury and Acute Kidney Injury.
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DOI：
10.1159/000520698
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发表时间：
2022
期刊：
影响因子：
2.5
通讯作者：
Bajwa, Amandeep
中科院分区：
文献类型：
--
作者：
Pabla, Navjot;Bajwa, Amandeep
急性肾损伤（AKI）是一种常见的临床疾病，与缺血性和肾毒性损伤导致的肾功能下降相关。 AKI 的病理生理学涉及多种细胞机制，例如肾实质细胞（上皮细胞和内皮细胞）功能障碍和免疫细胞浸润。线粒体损伤会导致 ATP 耗竭并引发细胞凋亡和坏死，这是缺血再灌注损伤 (IRI) 的核心。直接或间接保护线粒体完整性和功能的药理学（SS-31 或 MitoQ）、细胞（树突状细胞或间充质干细胞）或遗传策略已被证明可以减轻临床前模型中 IRI 相关的 AKI。有趣的是，最近显示分离的线粒体被各种哺乳动物细胞吸收，导致移植的线粒体掺入受体细胞的内源性线粒体网络，并有助于保护各种临床前缺血模型（包括心脏、肝脏和肾脏）免受缺血性损伤。小型综述总结了当前通过针对线粒体健康来改善肾功能的可用治疗策略。
Acute Kidney Injury (AKI) is a common clinical disorder associated with decline in renal function because of ischemic and nephrotoxic insults. The pathophysiology of AKI involves multiple cellular mechanisms, such as kidney parenchymal cell (epithelial and endothelial) dysfunction and immune cell infiltration. Mitochondrial injury which causes ATP depletion and triggers apoptosis, and necrosis is at the heart of Ischemia Reperfusion Injury (IRI). Pharmacological (SS-31 or MitoQ), cellular (dendritic cells or mesenchymal stem cells), or genetic strategies that either directly or indirectly preserve mitochondrial integrity and function have been shown to mitigate IRI linked AKI in preclinical models. Interestingly, isolated mitochondria have been recently shown to be taken up by various mammalian cells resulting in incorporation of transplanted mitochondria into the endogenous mitochondrial network of recipient cells and contributing to protection from ischemic injury in various preclinical models of ischemia including heart, liver, and kidneys. The mini review summarizes the current available therapeutic strategies that improve kidney function by targeting mitochondria health.
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