ArticleMolecular medicine reports2021
Sacubitril/valsartan (LCZ696) reduces myocardial injury following myocardial infarction by inhibiting NLRP3‑induced pyroptosis via the TAK1/JNK signaling pathway.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- Sacubitril/valsartan attenuates renal injury caused by cecal ligation and puncture via TLR4/NFκB/NLRP3 inhibition and reduced oxidative stress and apoptosis in rats.Scientific reports · 2026Article
- Sacubitril/Valsartan Ameliorates Inflammation and Oxidative Stress in Hypertensive Heart Disease by Upregulating CAMKK2 Protein and Modulating the AMPK/AKT/GSK-3β Axis.The Kaohsiung journal of medical sciences · 2026Article
- Molecular mechanisms underlying cyclophosphamide-induced ovarian injury and protective strategies.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Article
- Influence and molecular mechanism of cinnamaldehyde against ventricular arrhythmia via the TAK1-p38MAPK-NLRP3 pathway.Heart and vessels · 2025Article
- PANoptosis: a potential target of atherosclerotic cardiovascular disease.Apoptosis : an international journal on programmed cell death · 2025Review
- Therapeutic Potential of Gasdermin D-Mediated Myocardial Pyroptosis in Ischaemic Heart Disease: Expanding the Paradigm From Bench to Clinical Insights.Journal of cellular and molecular medicine · 2025Review
- Mechanisms and Therapeutic Potential of Multiple Forms of Cell Death in Myocardial Ischemia-Reperfusion Injury.International journal of molecular sciences · 2024Review
- The Role of Pyroptosis in Coronary Heart Disease.Anatolian journal of cardiology · 2024Article
- Punicalagin attenuates ventricular remodeling after acute myocardial infarction via regulating the NLRP3/caspase-1 pathway.Pharmaceutical biology · 2023Article
- Review
- Gasdermin D-mediated pyroptosis in myocardial ischemia and reperfusion injury: Cumulative evidence for future cardioprotective strategies.Acta pharmaceutica Sinica. B · 2023Review
- The history and mystery of sacubitril/valsartan: From clinical trial to the real world.Frontiers in cardiovascular medicine · 2023Review
- Sacubitril/valsartan in Heart Failure and Beyond-From Molecular Mechanisms to Clinical Relevance.Reviews in cardiovascular medicine · 2022Review
- Exosomes and Exosomal Cargos: A Promising World for Ventricular Remodeling Following Myocardial Infarction.International journal of nanomedicine · 2022Review
- Sacubitril Valsartan Enhances Cardiac Function and Alleviates Myocardial Infarction in Rats through a SUV39H1/SPP1 Axis.Oxidative medicine and cellular longevity · 2022Article
- The NLRP3 Inflammasome: Relevance in Solid Organ Transplantation.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study aimed to investigate the protective effects of sacubitril/valsartan (LCZ696) on ventricular remodeling in myocardial infarction (MI) and the effects of the inflammasome‑mediated inflammatory response. First, a rat model was established. Animals were then treated with LCZ696 so that the histopathological changes associated with ventricular remodeling could be investigated. The serum levels of the inflammatory factors IL‑18 and IL‑1β were also determined by ELISA. Immunofluorescence was used to investigate the ratio of pyroptosis following MI modelling. Western blotting and reverse transcription‑quantitative PCR were used to detect the relative expression levels of proteins and mRNAs in the transforming growth factor β‑activated kinase‑1 (TAK1)/JNK pathway and those associated with the NLR pyrin family domain containing 3 (NLRP3) inflammasome, respectively. The present study also investigated the regulatory mechanisms and associations between the TAK1 and JNK pathways, NOD‑, leucine‑rich repeat‑ and the NLRP3 inflammasome, in H9C2 cells and myocardial cells from the rat model of MI. LCZ696 improved MI‑induced myocardial fibrosis, rescued myocardial injury and suppressed the release of inflammatory factors. With regards to myocardial cell damage, pyroptosis in cardiomyocytes was observed. The
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.