Acute kidney injury (AKI) refers to a clinical syndrome caused by various factors that rapidly decrease renal function in a short period of time. In severe cases, it can progress to renal failure and even death. At present, there is no effective clinical treatment method for AKI. The pathogenic mechanism of AKI is relatively complex, with studies confirming its involvement in the pathological process of AKI, including inflammatory response, cell apoptosis, necrotic apoptosis, and ferroptosis. Connexin43 (Cx43) is a channel protein that participates in various signaling pathways and plays a role in promoting inflammation, apoptosis, necroptosis, and ferroptosis. Cx43 has recently been established as a participant in the development of kidney disease. It has been found that the expression of Cx43 changes in AKI induced by lipopolysaccharide, cisplatin, perfluorooctane sulfonic acid, and other etiologies. Therefore, inhibiting the expression of Cx43 is of great significance for the treatment of AKI. This article provides a systematic review of the structural functions, signaling pathways involved, and roles of Cx43 in acute kidney injury, and discusses the potential prospects for future treatment of acute kidney injury based on Cx43.

Dan Xia, Hong Li, Hongbao Liu. The role of gap junction protein 43 in acute kidney injury. International Journal of Frontiers in Medicine (2023), Vol. 5, Issue 10: 33-38. https://doi.org/10.25236/IJFM.2023.051006.

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