ArticleCardiovascular diabetology2025
Sacubitril/Valsartan partially alleviates myocardial infarction injury by activating the FGF21 signaling pathway via PPARs.
Article in Cardiovascular diabetology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Fibroblast Growth Factor 7 Limits Fibroblast-Driven Matrix Remodeling in Abdominal Aortic Aneurysm.Cardiovascular drugs and therapy · 2026Article
- Exercise-induced myokines in metabolic regulation: mechanisms, mimetics, and translational potential.Archives of pharmacal research · 2026Review
- Glabridin improves cardiac remodeling after myocardial infarction by activating PPARγ to regulate the ubiquitination and degradation of EGFR.Biology direct · 2026Article
- The effects of sacubitril/valsartan compared to valsartan in experimentally induced chronic kidney disease.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Early in-hospital initiation of angiotensin-receptor-neprilysin inhibitor in post-acute myocardial infarction patients with impaired left ventricular systolic function: a systematic review and meta-analysis of randomized controlled trials.Frontiers in cardiovascular medicine · 2026Article
- Early sacubitril/valsartan use associated with reduced atrial fibrillation risk in patients with acute myocardial infarction complicated by mitral regurgitation: a retrospective cohort study.Frontiers in cardiovascular medicine · 2025Article
- β-sitosterol ameliorates myocardial infarction injury via modulating the NF-κB and necroptosis signaling pathways.Frontiers in pharmacology · 2025Article
- Uncovering key biomarkers, potential therapeutic targets and development of deep learning model in heart failure.PloS one · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
The recent discovery of clinically significant data, alongside novel physiological and pathological occurrences surrounding sacubitril/valsartan (Sac/Val) beyond its approved indications, necessitates an urgent reevaluation of its underlying mechanism of action. In the present investigation, we observed a substantial elevation in the serum levels of fibroblast growth factor 21 (FGF21) among patients with acute myocardial infarction (AMI) who were administered Sac/Val, compared to those who were not, utilizing ELISA-based measurements. Furthermore, through the utilization of a mouse model of myocardial infarction induced by ligation of the left anterior descending branch, we confirmed that FGF21 mediates the cardioprotective effect of Sac/Val, employing both loss-of-function and gain-of-function approaches. Molecular docking and SPR experiments validated that Sac/Val can regulate FGF21 via its interaction with PPARs, and verified the role of PPARs in mediating Sac/Val regulation of FGF21 by inhibiting PPARs. In conclusion, we found that Sac/Val can act as an agonist of FGF21, which provides a new idea for the development of FGF21 drugs, and FGF21 as a new target of Sac/Val to ameliorate myocardial infarction, which provides a basis for new indications for Sac/Val.
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