IGFBP5 promotes EndoMT and renal fibrosis through H3K18 lactylation in diabetic nephropathy.

ABSTRACT:

Objective

Diabetic nephropathy (DN) is an important complication in diabetic patients that severely impacts their quality of life and life expectancy. Although metabolic and inflammatory responses induced by hyperglycemia are considered the primary pathogenic factors of DN, the specific molecular mechanisms involved remain unclear. Here, we investigated the role of insulin-like growth factor-binding protein 5 (IGFBP5) in DN using in vitro cell experiments and mouse models.

Methods

We assessed the effects of high-glucose conditions on IGFBP5 expression in glomerular endothelial cells and evaluated its regulatory effects on glycolysis, NLRP3 inflammasome activation, endothelial‒mesenchymal transition (EndoMT), and histone lactylation via the suppression of IGFBP5. Furthermore,

SUBMITTER: Hu X 

PROVIDER: S-EPMC12116956 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature