Role and mechanism of endoplasmic reticulum stress and NLRP3 inflammasome in acute kidney injury
10.11817/j.issn.1672-7347.2024.230301
- VernacularTitle:内质网应激和NLRP3炎症小体在急性肾损伤中的作用及其机制
- Author:
Mingxin PEI
1
;
Ke DENG
;
Yanling CHEN
Author Information
1. 遵义医科大学珠海校区病理生理学教研室,广东 珠海 519041
- Keywords:
endoplasmic reticulum stress;
Nod-like receptor family pyrin domain containing 3 inflammasome;
acute kidney injury;
unfolded protein response
- From:
Journal of Central South University(Medical Sciences)
2024;49(3):367-376
- CountryChina
- Language:Chinese
-
Abstract:
Acute kidney injury(AKI)is a common critical condition in clinical practice,characterized by a rapid decline in renal function within a short period.The pathogenesis of AKI is complex and has not been fully elucidated.In recent years,studies have found that the activation of endoplasmic reticulum stress(ERS)and the Nod-like receptor family pyrin domain containing 3(NLRP3)inflammasome are closely related to the occurrence of AKI.When the kidneys is damaged,the internal environment of the kidney cells is disrupted,leading to the activation of ERS.Excessive ERS can induce apoptosis of renal cells,leading to the occurrence of AKI.Additionally,the NLRP3 inflammasome can mediate the recognition of endogenous and exogenous danger signal molecules by the host,subsequently activating caspase-1,pro-inflammatory cytokines such as IL-1β and IL-18,inducing inflammatory responses,and promoting apoptosis of renal cells.In animal models of AKI,the upregulation of ERS markers is often accompanied by increased expression levels of NLRP3 inflammasome-related proteins,indicating that ERS can regulate the activation process of the NLRP3 inflammasome.Clarifying the role and mechanism of ERS and NLRP3 inflammasome in AKI is expected to provide new insights for the prevention and treatment of AKI.
