Autophagy is activated to protect against endotoxic acute kidney injury

Shuqin Mei, Man Jiang Livingston, Jielu Hao, Lin Li, Changlin Mei, Zheng Dong

Research output: Contribution to journalArticlepeer-review

44 Scopus citations

Abstract

Endotoxemia in sepsis, characterized by systemic inflammation, is a major cause of acute kidney injury (AKI) in hospitalized patients, especially in intensive care unit; however the underlying pathogenesis is poorly understood. Autophagy is a conserved, cellular catabolic pathway that plays crucial roles in cellular homeostasis including the maintenance of cellular function and viability. The regulation and role of autophagy in septic or endotoxic AKI remains unclear. Here we show that autophagy was induced in kidney tubular cells in mice by the endotoxin lipopolysaccharide (LPS). Pharmacological inhibition of autophagy with chloroquine enhanced LPS-induced AKI. Moreover, specific ablation of autophagy gene 7 (Atg7) from kidney proximal tubules worsened LPS-induced AKI. Together, the results demonstrate convincing evidence of autophagy activation in endotoxic kidney injury and support a renoprotective role of autophagy in kidney tubules.

Original languageEnglish (US)
Article number22171
JournalScientific reports
Volume6
DOIs
StatePublished - Feb 26 2016

ASJC Scopus subject areas

  • General

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