Hypoxia leads to the discovery of renal inflammation

Hypoxia leads to the discovery of renal inflammation

January 29, 2019 Source: Health News Network Author: Chengshou Qin

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Professor Liu Bicheng and Professor Lu Linli from the Zhongda Hospital affiliated to Southeast University conducted a series of studies to reveal for the first time a new mechanism of exosome-mediated hypoxic renal inflammatory injury, which provides a new target for the prevention and treatment of acute kidney injury based on exosomes. Recently, research papers were published online in the journal International Nephrology.

According to reports, acute kidney injury has a high mortality rate and is prone to develop chronic renal failure, and its pathogenesis is still not fully understood. Previous studies have shown that hypoxia is a key factor in the development of tubulointerstitial inflammation during acute kidney injury. Although hypoxia-inducible factor is the main regulator of hypoxia, the specific mechanism of regulation of renal tubulointerstitial inflammation remains. Not sure.

Renal tubular epithelial cells are particularly susceptible to ischemia, hypoxia, and metabolic damage. The research team found through a series of studies that renal tubular epithelial cells can secrete exosomes and transmit damage signals to various stress injuries. Adjacent or distant cells promote the occurrence of kidney damage. In this study, through systematic animal models and cell culture studies, it was confirmed that under hypoxic conditions, hypoxia-inducible factors can promote the secretion of miRNA-23a-rich exosomes from tubular epithelial cells, and can be taken up by macrophages to inhibit pan-inhibition. The activity of the protein editing protein A20 induces a proinflammatory response of macrophages, thereby promoting the occurrence of tubulointerstitial inflammation.

Li Zuolin, a doctoral student in the Department of Nephrology, Southeast University, and the Department of Nephrology, Zhongda Hospital, Southeast University, is the first author of the paper. The research was funded by the National Natural Science Foundation's major international cooperation projects and face projects, and the Jiangsu Provincial Kidney Disease Clinical Research Center.

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