LncRNA nonnmmut065573 promotes post-myocardial infarction cardiac fibrosis and activates the TGF-β1/ZEB1 pathway.

ABSTRACT: Cardiac fibrosis following myocardial infarction (MI) is a critical determinant of progressive cardiac dysfunction, yet the underlying mechanisms driving this pathological process remain incompletely understood. Elucidating these regulatory pathways holds profound implications for improving post-MI prognosis.Our prior work demonstrated that chronic intermittent hypoxia (CIH) exacerbates cardiac fibrosis while modulating the expression of long non-coding RNA (lncRNA) nonnmmut065573 (tentatively designated LncRNA-IH) in cardiac tissues. Herein, we sought to determine the role of LncRNA-IH in post-MI cardiac fibrosis and its underlying mechanisms. Using a C57BL/6 mouse model of MI, we established a mouse model with cardiac-specific overexpression of LncRNA-IH to evaluate post-MI cardiac fibro

SUBMITTER: Hu C 

PROVIDER: S-EPMC12824076 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature