LncRNA SNHG8 contributes to post-myocardial infarction cardiac fibrosis and is functionally associated with miR-192-3p.

Cardiac fibrosis is a major contributor to adverse ventricular remodeling after myocardial infarction (MI), but the non-coding RNA networks involved in fibroblast responses remain incompletely understood. We investigated the role of the long non-coding RNA SNHG8 in post-infarction cardiac fibrosis and its relationship with miR-192-3p using a murine MI model and angiotensin II (Ang II)-stimulated cardiac fibroblasts. SNHG8 expression was significantly increased in infarcted myocardium and in Ang II-treated fibroblasts. SNHG8 silencing reduced fibroblast proliferation and the expression of α-smooth muscle actin and collagen I, whereas SNHG8 overexpression produced the opposite effects in cultured fibroblasts. Dual-luciferase and rescue experiments supported a functional relationship between SNHG8 and miR-192-3p in vitro; however, these experiments do not establish an endogenous ceRNA mechanism or a validated downstream effector. In vivo, SNHG8 knockdown reduced post-MI scar burden and collagen I-positive area and partially preserved left ventricular systolic function. The role of miR-192-3p in mediating these in vivo effects was not tested. Together, the findings support a profibrotic role for SNHG8 in experimental post-MI remodeling and identify the SNHG8-miR-192-3p relationship as a candidate mechanism requiring further biochemical and in vivo validation.