Key result
Cardiac Erbb4-IR silencing improves cardiac function and blunts Ang II-induced fibrosis in mice.
Why the study?
The role of the lncRNA Erbb4-IR in hypertensive heart disease remains unexplored.
Does silencing cardiac Erbb4-IR improve cardiac function and reduce cardiac fibrosis in Angiotensin II-induced hypertensive mice?
Population
Hypertensive mice induced by angiotensin II
Comparison
Silencing of cardiac Erbb4-IR vs unsilenced angiotensin II control
Design
Preclinical animal study
Authors
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May identify Erbb4-IR as a target in hypertensive remodeling; leaves open translation from mouse models to clinical use.
Does silencing cardiac Erbb4-IR improve cardiac function and reduce cardiac fibrosis in Angiotensin II-induced hypertensive mice?
p-value: p=<0.01
Silencing the long non-coding RNA Erbb4-IR protects against Angiotensin II-induced cardiac remodeling and fibrosis, suggesting it as a potential therapeutic target for hypertensive heart disease.
Li et al. (2023) studied Hypertensive heart disease and cardiac fibrosis. Erbb4-IR shRNA vs. Empty vector (EV) or saline was evaluated on Cardiac dysfunction and fibrosis (LVEF, LVFS, LV mass, and collagen accumulation) (p=<0.01). Silencing cardiac Erbb4-IR by shRNA gene transfer significantly improved Angiotensin II-induced cardiac dysfunction and inhibited progressive cardiac fibrosis in a mouse model.
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