M⁶A modification regulates lung fibroblast-to-myofibroblast transition through modulating KCNH6 mRNA translation.

ABSTRACT: Idiopathic pulmonary fibrosis (IPF) is a chronic, fatal lung disease characterized by progressive and non-reversible abnormal matrix deposition in lung parenchyma. Myofibroblasts originating mainly from resident fibroblasts via fibroblast-to-myofibroblast transition (FMT) are the dominant collagen-producing cells in pulmonary fibrosis. N⁶-methyladenosine (m⁶A) modification has been implicated in various biological processes. However, the role of m⁶A modification in pulmonary fibrosis remains elusive. In this study, we reveal that m⁶A modification is upregulated in a bleomycin (BLM)-induced pulmonary fibrosis mouse model, FMT-derived myofibroblasts, and IPF patient lung samples. Lowering m⁶A levels through silencing methyltransferase-li

SUBMITTER: Zhang JX 

PROVIDER: S-EPMC8636177 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature