TIMP2 protects against sepsis-associated acute kidney injury by cAMP/NLRP3 axis-mediated pyroptosis

Author:

Xu Dongxue1,Jiang Jun1,Liu Ye1,Pang Jingjing1,Suo Jinmeng1,Li Yiming1,Peng Zhiyong1234ORCID

Affiliation:

1. Department of Critical Care Medicine, Zhongnan Hospital of Wuhan University, Wuhan, China

2. Clinical Research Center of Hubei Critical Care Medicine, Wuhan, China

3. Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States

4. Intensive Care Unit of the second affiliated Hospital of Hainan Medical College, Haikou, China

Abstract

Tissue inhibitor of metalloproteinase 2 (TIMP-2) has been found to be the best biomarker for predicting the risk of sepsis-associated acute kidney injury (SA-AKI). However, its role and the underlying mechanism in SA-AKI remain elusive. The authors demonstrated in this study using kidney tubule-specific knockout mice model of SA-AKI and primary renal tubule cells stimulated with lipopolysaccharide (LPS) that extracellular TIMP-2 promoted NOD-like receptor protein 3 (NLRP3) ubiquitination and autophagy-dependent degradation by increasing intracellular cyclic adenosine monophosphate (cAMP), thus attenuated pyroptosis and alleviated renal damage.

Funder

MOST | NSFC | Excellent Young Scientists Fund

MOST | National Natural Science Foundation of China

Publisher

American Physiological Society

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