Systemic miR-26a deficiency attenuates pulmonary fibrosis via PTEN upregulation and downstream TIMP-1 suppression.

ABSTRACT: Several microRNAs (miRNAs) have been implicated in the pathophysiology of pulmonary fibrosis; however, the detailed mechanisms remain unclear. miR-26a has demonstrated antifibrotic effects, particularly when its expression is suppressed in the airways. However, the effects of systemic miR-26a deficiency on pulmonary fibrosis have not been investigated. We found that miR-26a knockout (KO) mice exhibited reduced pulmonary fibrosis compared with wild-type (WT) mice. Whole-lung RNA sequencing analysis indicated that the mammalian target of rapamycin complex 1 (MTORC1) signaling and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathways were elevated in the WT group compared with the KO group. Loss of miR-26a increases PTEN expression, a target gene of miR-26a, resultin

SUBMITTER: Hamada A 

PROVIDER: S-EPMC12663618 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature