急性肾损伤中的线粒体
Mitochondria in Acute Kidney Injury.
作者信息
Ralto Kenneth M, Parikh Samir M
机构信息
Division of Nephrology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA.
Division of Nephrology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA.
出版信息
Semin Nephrol. 2016 Jan;36(1):8-16. doi: 10.1016/j.semnephrol.2016.01.005.
Abstract
Acute kidney injury (AKI) continues to be a significant contributor to morbidity, mortality, and health care expenditure. In the United States alone, it is estimated that more than $10 billion is spent on AKI every year. Currently, there are no available therapies to treat established AKI. The mitochondrion is positioned to be a critical player in AKI with its dual role as the primary source of energy for each cell and as a key regulator of cell death. This review aims to cover the current state of research on the role of mitochondria in AKI, while also proposing potential therapeutic targets and future therapies.
摘要
急性肾损伤（AKI）仍然是导致发病率、死亡率和医疗保健支出的重要因素。仅在美国，据估计每年在AKI上的花费就超过100亿美元。目前，尚无可用的疗法来治疗已确诊的AKI。线粒体作为每个细胞的主要能量来源以及细胞死亡的关键调节因子，在AKI中起着至关重要的作用。本综述旨在涵盖线粒体在AKI中作用的当前研究状况，同时提出潜在的治疗靶点和未来疗法。
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