ArticleCardiovascular diagnosis and therapy2021
Long non-coding RNA SENCR alleviates hypoxia/reoxygenation-induced cardiomyocyte apoptosis and inflammatory response by sponging miR-1.
Article in Cardiovascular diagnosis and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 19 citations in OpenAlex.
- Sevoflurane attenuates hypoxia/reoxygenation-induced cardiomyocyte injury via the LncRNA FAM201A/miR-488-3p/PTEN axis.BMC anesthesiology · 2025Article
- Promising roles of non-exosomal and exosomal non-coding RNAs in the regulatory mechanism and as diagnostic biomarkers in myocardial infarction.Journal of Zhejiang University. Science. B · 2023Review
- Non-coding RNAs in the pathophysiology of heart failure with preserved ejection fraction.Frontiers in cardiovascular medicine · 2023Review
- Long Noncoding RNAs Involved in Cardiomyocyte Apoptosis Triggered by Different Stressors.Journal of cardiovascular translational research · 2022Review
- Article
- Epigenetic regulation in myocardial infarction: Non-coding RNAs and exosomal non-coding RNAs.Frontiers in cardiovascular medicine · 2022Review
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4 authors at 1 institution in 1 country.
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Abstract
backgroundMyocardial cell apoptosis is one of the main reasons for the occurrence of acute myocardial infarction (AMI). The role of smooth muscle and endothelial cell enriched migration/differentiation-associated lncRNA (SENCR) in the cardiomyocyte apoptosis induced by hypoxia/reoxygenation (H/R) injury and its potential mechanism were investigated in this study to provide a novel biomarker for the development of AMI.
methodsThe expression levels of SENCR in the serum of AMI patients and non-AMI patients with chest pain (control) were detected by qRT-PCR. The function of SENCR in the cardiomyocyte apoptosis and inflammatory response induced by H/R injury was evaluated by MTT, cell apoptosis, and ELISA assay, respectively. The mechanism underlying the function of SENCR was investigated with the luciferase reporter assay.
resultsSENCR was significantly downregulated in AMI compared with the control volunteers, which showed negative correlations with the cardiac troponin I (cTnI) and creatine kinase-MB (CK-MB) level of patients. The H/R injury-induced cell apoptosis and inflammatory response in cardiomyocytes, which were attenuated by the overexpression of SENCR. The expression of miR-1 was suppressed by the overexpression of SENCR, while the overexpression of miR-1 could alleviate the cell apoptosis, enhance cell viability, and attenuate inflammatory response in cardiomyocyte. SENCR reversed H/R-induced myocardial cell injury by regulating the expression of miR-1.
conclusionsSENCR was correlated with the clinicopathological features of patients and was revealed to alleviate the cardiomyocyte apoptosis and inflammatory response induced by H/R injury via sponging miR-1.
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