inhibition of ltbp2 suppresses high glucose-induced proliferation, fibrosis, and inflammation in glomerular mesangial cells by disrupting the pi3k/akt/nf-κb pathway

Latent transforming growth factor-β binding protein-2 (ltbp2) plays a significant role in tissue fibrosis. this research aimed to elucidate whether ltbp2 influences the progression of diabetic nephropathy (dn) through the phosphatidylinositol 3-kinases/protein kinase b (pi3k/akt)/nuclear factor kappa-b (nf-κb) pathway.the hbzy-1 cells were exposed to high glucose to create diabetic nephropathy cell model. ltbp2 levels were examined by western blot and immunofluorescence. after verifying the transfection efficiency of si-ltbp2, cell counting kit-8, 5-ethynyl-2-deoxyuridine staining, western blot, flow cytometry and immunofluorescence were utilized to assess the proliferation, apoptosis and fibrosis of hbzy-1 cells, respectively. collagen deposition was also detected by sirius red staining, and inflammatory factors levels were determined by elisa. pi3k/akt/nf-κb pathway activators were applied to explore whether ltbp2 silencing could play a role in dn by modulating this pathway.after treatment with high glucose, the expression of ltbp2 was elevated in hbzy-1 cells. ltbp2 silencing hindered the aberrant proliferation of hbzy-1 cells, with no significant effect on apoptosis; meanwhile, it reduced fibrosis, decreased collagen content, and decreased inflammatory factors levels in hbzy-1 cells. following treatment with high glucose, the pi3k, akt, and p65 phosphorylation levels were increased, whereas silencing ltbp2 reduced them. activators of the pi3k/akt/nf-κb pathway weakened the inhibition of ltbp2 silencing on cell proliferation, fibrosis, and inflammation.in conclusion, silencing of ltbp2 weakened the proliferation, fibrosis, and inflammation of hbzy-1 cells treated with high glucose by hindering the pi3k/akt/nf-κb pathway. this research offers a new reference for the targeted therapy of dn.