ArticleAmerican journal of translational research2022
Angiotensin receptor-neprilysin inhibitor attenuates ischemia-hypoxia-induced myocardial injury via inhibition of autophagy.
Article in American journal of translational research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed, 3 citations in OpenAlex.
- Exploring the Potential Effects and Mechanism of Astragalus Membranaceus in Treating Ischemic Heart Failure Based on Network Pharmacology and Experimental Verification.Combinatorial chemistry & high throughput screening · 2025Article
- Protein homeostasis in the aged and diseased heart.The journal of cardiovascular aging · 2023Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
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Abstract
objectivesAngiotensin receptor-neprilysin inhibitor (ARNI) improves cardiac function and protects from an ischemic myocardium. However, the role and mechanism of ARNI on autophagy in cardiac ischemic injury are poorly understood. Here, we investigated the protective effect and underlying mechanisms of ARNI on autophagy in H9c2 cardiomyocytes induced through ischemia and hypoxia (IH) treatment.
methodsThe cytotoxicity of IH injury on H9C2 cells with and without ARNI were evaluated using cell counting kit-8 (CCK-8) and lactate dehydrogenase (LDH) release assays. The effect of ARNI on apoptosis was detected using flow cytometry. The expression of autophagic proteins (LC3-II, Beclin 1, and p62) was detected using western blot.
resultsThe viability of H9c2 cells was significantly decreased at different IH-treated time points; ARNI pretreatment increased cell viability and inhibited IH injury in a dose-dependent manner. H9c2 cells treated with IH (6 h) significantly increased LDH release, while ARNI dose-dependently improved LDH release, with 20 μmol/L ARNI having the most significant effect. ARNI also ameliorated IH-induced apoptosis. IH treatment increased the protein expression of LC3-II and Beclin 1 and decreased the expression of p62, which were reversed by ARNI pretreatment. Furthermore, autophagy was further increased after pretreatment with rapamycin in IH-induced H9c2 cells, which abrogated the protective effect of ARNI.
conclusionsOur study shows that ARNI has a protective effect on IH-induced cardiomyocyte injury, which may be related to the inhibition of autophagy.
Indexed as
Identifiers
36628240PMC9827305W4315619220What OpenQuestion holds
Registered trials
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.