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Review
. 2024 Nov;48(11):1621-1624.
doi: 10.1002/cbin.12240. Epub 2024 Sep 9.

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

Zhixiong Wu  1 , Wei Qing Liu  1 , Liang Tang  1 , Qiong Yuan  1 , Yaling Li  1 , Hongyu Hu  1 , Xin Luo  1 , Fan Ouyang  1
Affiliations
Review

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

Zhixiong Wu et al. Cell Biol Int. 2024 Nov.

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.

Keywords: acute kidney injury; lactate; lactonization; mitochondrial; sepsis.

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References

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