ArticleBiomedical engineering online2020
Inhibition of miR-153 ameliorates ischemia/reperfusion-induced cardiomyocytes apoptosis by regulating Nrf2/HO-1 signaling in rats.
Article in Biomedical engineering online, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.
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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
14 citing papers in PubMed, 28 citations in OpenAlex.
- MiR-153 is Involved in Testicular Ischemia/Reperfusion Injury by Directly Targeting FOXO3 and Regulating Spermatogonia Pyroptosis.Molecular biotechnology · 2025Article
- Protective effect of canagliflozin on post-resuscitation myocardial function in a rat model of cardiac arrest.Intensive care medicine experimental · 2023Article
- Heme Oxygenase-1 and Its Role in Colorectal Cancer.Antioxidants (Basel, Switzerland) · 2023Review
- MicroRNA profiling of the feline left heart identifies chamber-specific expression signatures in health and in advanced hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology plus · 2023Article
- MicroRNA-214-3p protects against myocardial ischemia-reperfusion injury by targeting demethylase lysine demethylase 3A.Regenerative therapy · 2023Article
- Acacetin alleviates myocardial ischaemia/reperfusion injury by inhibiting oxidative stress and apoptosis via the Nrf-2/HO-1 pathway.Pharmaceutical biology · 2022Article
- The activation of SIRT3 by dexmedetomidine mitigates limb ischemia-reperfusion-induced lung injury.Annals of translational medicine · 2022Article
- Comprehensive overview of Nrf2-related epigenetic regulations involved in ischemia-reperfusion injury.Theranostics · 2022Review
- The Antioxidant Transcription Factor Nrf2 in Cardiac Ischemia-Reperfusion Injury.International journal of molecular sciences · 2021Review
- Review
- miR-3587 Inhibitor Attenuates Ferroptosis Following Renal Ischemia-Reperfusion Through HO-1.Frontiers in molecular biosciences · 2021Article
- Correction to: Inhibition of miR‑153 ameliorates ischemia/reperfusion‑induced cardiomyocytes apoptosis by regulating Nrf2/HO‑1 signaling in rats.Biomedical engineering online · 2020Article
- The Effects of Hypoxia-Reoxygenation in Mouse Digital Flexor Tendon-Derived Cells.Oxidative medicine and cellular longevity · 2020Article
- Role of Nrf2 and Its Activators in Cardiocerebral Vascular Disease.Oxidative medicine and cellular longevity · 2020Review
Corrections and comments
- Erratum issuedCorrection to: Inhibition of miR‑153 ameliorates ischemia/reperfusion‑induced cardiomyocytes apoptosis by regulating Nrf2/HO‑1 signaling in rats.2020 · Map, Jiaguo [corrected to Ma, Jiaguo]
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPrevious in vitro studies demonstrated that suppression of microRNAs might protect cardiomyocytes and neurons against oxygen-glucose deprivation and reoxygenation (OGD/R)-induced cell apoptosis. However, whether the protective effect of miR-153-inhibition on cardiomyocytes can be observed in the animal model is unknown. We aimed to address this question using a rat model of ischemia-reperfusion (I/R).
methodsRats were received the intramyocardial injection of saline or adenovirus-carrying target or control gene, and the rats were subjected to ischemia/reperfusion (I/R) treatment. The effects of miR-153 on I/R-induced inflammatory response and oxidative stress in the rat model were assessed using various assays.
resultsWe found that suppression of miR-153 decreased cleaved caspase-3 and Bcl-2-associated X (Bax) expression, and increased B cell lymphoma 2 (Bcl-2) expression. We further confirmed that Nuclear transcription factor erythroid 2-like 2 (Nrf2) is a functional target of miR-153, and Nrf2/Heme oxygenase-1 (HO-1) signaling was involved in miR-153-regulated I/R-induced cardiomyocytes apoptosis. Inhibition of miR-153 reduced I/R-induced inflammatory response and oxidative stress in rat myocardium.
conclusionSuppression of miR-153 exerts a cardioprotective effect against I/R-induced injury through the regulation of Nrf2/HO-1 signaling, suggesting that targeting miR-153, Nrf2, or both may serve as promising therapeutic targets for the alleviation of I/R-induced injury.
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