ArticleBiomedical reports2013
Inhibition of ubiquitin protein expression and 20S proteasome activity by irbesartan prevents post-infarction ventricular remodeling and decreases TNF-α generation.
Article in Biomedical reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 6 citations in OpenAlex.
- Endothelial dysfunction in plaque rupture and plaque erosion.Heart and vessels · 2026Article
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9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial infarction (MI) may induce severe alterations of the cardiac contractile function that may, in turn, lead to heart failure (HF). The ubiquitin-proteasome system (UPS) plays a critical role in cardiac remodeling following MI. Angiotensin II type 1 receptor (AT1R) blockers effectively prevent left ventricular (LV) remodeling. However, it has not been elucidated whether the preventive effect of AT1R-blockers on LV remodeling is mediated through the UPS pathway. In the present study, with the use of cardiac morphometric parameters, haemodynamic measurements and enzyme-linked immunosorbent assay, we demonstrated that post-ischemic HF rats exhibited a significant increase in ventricular remodeling and irbesartan was effective in reversing cardiac remodeling. The expression of TNF-α, ubiquitin protein and 20S proteasome were significantly increased in the MI control group and irbesartan was shown to dose-dependently inhibit the expression of TNF-α, ubiquitin protein and 20S proteasome. In conclusion, it was hypothesized that UPS signaling is involved in ventricular remodeling following MI and the mechanism underlying the effect of irbesartan on ventricular remodeling may be associated with the downregulation of the expression of TNF-α, ubiquitin protein and 20S proteasome.
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