SNHG8 plays a profibrotic role in experimental post-MI remodeling and its functional relationship with miR-192-3p represents a candidate mechanism requiring further biochemical and in vivo validation.
SNHG8 expression was significantly elevated in infarcted myocardium and in Ang II-stimulated cardiac fibroblasts.
SNHG8 silencing reduced cardiac fibroblast proliferation and decreased expression of fibrotic markers alpha-smooth muscle actin and collagen I.
Dual-luciferase and rescue experiments supported a functional relationship between SNHG8 and miR-192-3p in vitro.
In vivo SNHG8 knockdown reduced post-MI scar burden and collagen I-positive area and partially preserved left ventricular systolic function.
The SNHG8-miR-192-3p relationship was identified as a candidate mechanism but was not validated in vivo.
This research suggests that a long non-coding RNA molecule called SNHG8 plays an important role in the scarring of heart tissue (cardiac fibrosis) that occurs after a heart attack. In both a mouse model of heart attack and in heart cells grown in the laboratory, SNHG8 levels rose significantly. When the researchers artificially reduced SNHG8 activity, heart cells were less likely to multiply and produce proteins associated with scar tissue formation, while increasing SNHG8 had the opposite effect. In mice that had experienced a heart attack, reducing SNHG8 led to smaller scars, less collagen accumulation, and some preservation of the heart's pumping ability. The study also explored a potential connection between SNHG8 and a small RNA molecule called miR-192-3p, using laboratory tests that suggested the two interact functionally. However, the researchers were careful to note that these experiments alone do not prove that SNHG8 works by 'sponging' or blocking miR-192-3p in living tissue, and no specific downstream target gene was confirmed. The connection between SNHG8 and miR-192-3p was not tested in the animal model. This research suggests that SNHG8 could be a potential target for future therapies aimed at reducing harmful heart scarring after a heart attack. However, the mechanisms by which SNHG8 exerts its effects remain incompletely understood, and further studies are needed to confirm whether the SNHG8-miR-192-3p relationship operates in the same way in living organisms before any clinical implications can be drawn.
Yang C, Li M, Su T, Jia D, Gao H, Guo H, et al.. (2026). LncRNA SNHG8 contributes to post-myocardial infarction cardiac fibrosis and is functionally associated with miR-192-3p.. Journal of molecular histology. https://doi.org/10.1007/s10735-026-10999-6