MiR-423-5p/NDUFS7-mediated mitochondrial function modulation contributes to quercetin-induced attenuation of pulmonary fibrosis via extracellular matrix remodeling regulation.

ABSTRACT:

Background

Idiopathic pulmonary fibrosis (IPF) is a type of interstitial lung disease that is critically influenced by epigenetic regulation and mitochondrial function during its pathogenesis and progression. Flavonoids possess significant anti-inflammatory and antioxidant properties, and among these compounds, quercetin has been shown to inhibit the progression of pulmonary fibrosis by modulating the expression of specific microRNAs (miRNAs) and alleviating oxidative stress associated with mitochondrial dysfunction. However, the precise underlying mechanism remains unclear.

Methods

We established a murine model of pulmonary fibrosis via endotracheal nebulization with bleomycin, which resulted in uniformly distributed, severe fibrotic lesions in the lungs. Quercetin (Que) wa

SUBMITTER: Xia L 

PROVIDER: S-EPMC12860696 | biostudies-literature | 2026 Jun

REPOSITORIES: biostudies-literature