Mindin deficiency alleviates renal fibrosis through inhibiting NF-κB and TGF-β/Smad pathways.

ABSTRACT: Renal fibrosis acts as a clinical predictor in patients with chronic kidney disease and is characterized by excessive extracellular matrix (ECM) accumulation. Our previous study suggested that mindin can function as a mediator for liver steatosis pathogenesis. However, the role of mindin in renal fibrosis remains obscure. Here, tumour necrosis factor (TGF)-β-treated HK-2 cells and global mindin knockout mouse were induced with renal ischaemia reperfusion injury (IRI) to test the relationship between mindin and renal fibrosis. In vitro, mindin overexpression promoted p65-the hub subunit of the NF-κB signalling pathway-translocation from the cytoplasm into the nucleus, resulting in NF-κB pathway activation in TGF-β-treated HK-2 cells. Meanwhile, mindin activated the TGF-β/Smad pathway, there

SUBMITTER: Yang K 

PROVIDER: S-EPMC7214143 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature