ArticleInternational journal of clinical and experimental pathology2017
Mir-23a inhibition attenuates ischemic/reperfusion-induced myocardial apoptosis by targeting XIAP.
Article in International journal of clinical and experimental pathology, 2017. 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, 7 citations in OpenAlex.
- The Wound-Heart Axis: Can Chronic Wounds Contribute to Cardiac Dysfunction?International journal of molecular sciences · 2026Review
- Exosomal miRNAs Mediate Immune-Metabolic Interactions in the Hemocytes of the Pearl OysterAnimals : an open access journal from MDPI · 2025Article
- Novel XIAP mutation with early-onset Crohn's disease complicated with acute heart failure: a case report.BMC cardiovascular disorders · 2023Article
- Suppression of RBFox2 by Multiple MiRNAs in Pressure Overload-Induced Heart Failure.International journal of molecular sciences · 2023Article
- Changes in miR 21 and 23b expression in postnatal hypertrophic heart derived from gestational diabetes precede dilated cardiomyopathy.Journal of biosciences · 2021Article
- Value of Serum miR-23a, miR-30d, and miR-146a Biomarkers in ST-Elevation Myocardial Infarction.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs are a group of single-strand, non-coding RNAs that inhibit the translation of protein-coding genes. Recent studies indicated that miRNAs are broadly involved in the development of cardiovascular diseases, including arrhythmia, hypertrophy, heart failure and cardiac injury. In this study, we report that miR-23a, a tumor suppressor, acts as an apoptotic promoter in rats undergoing ischemic/reperfusion. In rats subjected to ischemic/reperfusion injury, the expression of miR-23a in heart tissue was upregulated significantly. The infarct area and the apoptosis rate also increased. In contrast, knockdown of miR-23a by tail injection of antagomir-23a attenuated the ischemic/reperfusion injury. Moreover, we used Western blots to determine that miR-23a targeted XIAP to influence the expression of caspase and the NFkB pathway. In summary, miR-23a was shown to be part of a novel regulatory pathway that contributed to ischemic/reperfusion injury.
Indexed as
Identifiers
31966373PMC6965768W3012436222What 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.