Succinate aggravates pulmonary fibrosis through the succinate/SUCNR1 axis.

ABSTRACT: Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease that leads to destruction of alveoli and replacement by fibrotic tissue. Metabolic profiling of lung tissue and serum from patients with IPF has revealed that levels of tricarboxylic acid cycle metabolites such as succinate are altered in patients with IPF. In our study, we aim to evaluate the role of succinate and its receptor-succinate receptor 1 (SUCNR1) in the pathogenesis of lung fibrosis, with a focus on fibroblasts, a central cell in IPF. SUCNR1 expression was investigated by using Western blots, qPCR, and in situ hybridisation. In vitro assays with IPF and normal human lung fibroblasts (NHLF) were used to evaluate the effect of succinate treatment on the expression of fibrotic markers, fibroblast-myofibroblas

SUBMITTER: Rajesh R 

PROVIDER: S-EPMC7617945 | biostudies-literature | 2025 May

REPOSITORIES: biostudies-literature