Key result
Propofol mitigates hypoxia/reoxygenation cardiomyocyte damage by suppressing miR-511-3p and restoring ATP2A2.
Why the study?
The role of microRNA-511-3p in cardiac injury and its involvement in propofol-mediated cardioprotection against hypoxia/reoxygenation injury was unclear.
Does propofol alleviate hypoxia/reoxygenation-induced injury in H9c2 cardiomyocytes?
Does propofol alleviate hypoxia/reoxygenation-induced injury in H9c2 cardiomyocytes?
Propofol protects cardiomyocytes against hypoxia/reoxygenation injury by suppressing miR-511-3p, which in turn restores the protective expression of ATP2A2, revealing a novel upstream epigenetic mechanism for its cardioprotective effects.
Answers are grounded in this paper and cite their sources.
In vitro results preclude altering propofol use in cardiac procedures; leaves open whether miR-511-3p/ATP2A2 modulation confers clinical cardioprotection.
Background Propofol (PPF) alleviates myocardial ischemia/reperfusion injury (MIRI), yet no existing studies have clarified the function of microRNA‐511‐3p (miR‐511‐3p) in cardiac injury or its link to PPF′s cardioprotection. Purpose This study clarified how the miR‐511‐3p/ATPase sarcoplasmic/endoplasmic reticulum Ca 2+ transporting 2 (ATP2A2) signaling cascade mediated PPF‐induced relief against hypoxia/reoxygenation (H/R) cardiac damage. Methods H/R damage models were established in H9c2 cells. Cell viability was measured via the CCK‐8 assay, and flow cytometry was used to quantify the proportion of apoptotic cells. Cellular reactive oxygen species (ROS) levels were assessed using the DCFH‐DA fluorescent staining method. ELISA and colorimetric tests were combined to measure cardiac injury markers, inflammatory mediators, and oxidative stress‐related molecules. RT‐qPCR was applied to test the expression levels of miR‐511‐3p and ATP2A2. Dual‐luciferase reporter assays were carried out to confirm the direct binding interaction between the two molecules. Results PPF markedly boosted the viability and restrained apoptosis of H9c2 cells subjected to H/R treatment. It also reduced the release of cardiac injury markers and eased excessive oxidative stress and inflammatory responses. H/R exposure raised miR‐511‐3p abundance, an alteration that PPF treatment could reverse. Forced miR‐511‐3p expression partially abolished the cardioprotective benefits brought by PPF. ATP2A2 was verified as a direct target of miR‐511‐3p, whose expression was suppressed by this miRNA. Upregulating ATP2A2 counteracted cell damage triggered by miR‐511‐3p overexpression. Conclusions PPF might mitigate H/R‐triggered cardiomyocyte damage, possibly through inhibiting miR‐511‐3p and increasing its target ATP2A2, and this molecular axis may offer a tentative therapeutic reference for MIRI.
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Sun et al. (2026) studied Myocardial ischemia/reperfusion injury. Propofol vs. Hypoxia/reoxygenation without propofol was evaluated on Cell viability (p=<0.001). Propofol significantly restored cell viability (p < 0.001) and mitigated hypoxia/reoxygenation-triggered cardiomyocyte damage by inhibiting miR-511-3p and increasing its target ATP2A2.
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