ArticleOxidative medicine and cellular longevity2022
miR-340-5p Alleviates Oxidative Stress Injury by Targeting MyD88 in Sepsis-Induced Cardiomyopathy.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- MicroRNAs as regulators of cardiac dysfunction in sepsis: pathogenesis and diagnostic potential.Frontiers in cardiovascular medicine · 2025Pooled it
- miR-222-3p targeting MEGF9 exacerbates sepsis-induced myocardial injury.Journal of cardiothoracic surgery · 2026Article
- Epigenetic alterations in type 1 diabetes and their association with poor glycemic control: the SED1-EPI substudy.Scientific reports · 2026Article
- Mechanisms and therapeutic strategies of copper homeostasis in the pathogenesis of sepsis-induced cardiomyopathy.Frontiers in cell and developmental biology · 2026Review
- Article
- Silencing of Cholesterol 25-Hydroxylase Attenuates Lipopolysaccharide-Induced Cardiomyocyte Damage In Vitro.Journal of cellular and molecular medicine · 2025Article
- miR-340-5p alleviates the damage effect of LPS on nucleus pulposus cells by negatively regulating the expression of SOX4.Journal of orthopaedic surgery and research · 2025Article
- Dysregulation of LINC01094 is involved in the pathogenesis of pulpitis by regulating the miR-340-5p expression.Odontology · 2025Article
- Sepsis-induced cardiac dysfunction: mitochondria and energy metabolism.Intensive care medicine experimental · 2025Review
- Research Progress of Macromolecules in the Prevention and Treatment of Sepsis.International journal of molecular sciences · 2023Review
- Glutathione system enhancement for cardiac protection: pharmacological options against oxidative stress and ferroptosis.Cell death & disease · 2023Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Sepsis-induced cardiomyopathy (SIC) is a sort of severe disease in the intensive care unit. This research focuses on exploring the influence of miR-340-5p on SIC and its specific mechanism. Methods: Mice were administered with lipopolysaccharide (LPS) to construct a SIC animal model. Mice were intramyocardially injected with Adenoassociated Virus- (AAV-) 9 containing the miR-340-5p precursor to make the miR-340-5p overexpression in the myocardium. The expression level of myocardial miR-340-5p was evaluated by qRT-PCR. The cardiac function was measured by echocardiography, the myocardial morphology was observed by hematoxylin-eosin (HE) staining, and the oxidative stress level was detected by 4-hydroxynonenal (4-HNE) immunohistochemical staining and malondialdehyde (MDA) assay in mice. The cells were pretreated with miR-340-5p mimic, mimic-NC, miR-340-5p inhibitor, inhibitor-NC, MyD88 siRNA, or si-NC and then administered with LPS or PBS. The cell viability was measured with the CCK-8 assay. The level of intracellular oxidative stress was evaluated using reactive oxygen species (ROS), MDA, and glutathione (GSH) detection. The MyD88 level was assessed via Western blotting analysis. The interaction of miR-340-5p with the MyD88 mRNA was confirmed via dual-luciferase reporter assay and RNA pull-down assay. Results: The miR-340-5p overexpression partially alleviated the increase of the MyD88 level, impairment of cardiac function, and oxidative stress injury in the SIC animal model. In the SIC cell model, miR-340-5p mimic pretreatment partially relieved oxidative stress injury, while the miR-340-5p inhibitor had the opposite effect. Besides, the miR-340-5p mimic and inhibitor could reduce and further increase the MyD88 level in the SIC cell model, respectively. Dual-luciferase reporter and RNA pull-down experiments confirmed the interaction between the MyD88 mRNA and miR-340-5p. Finally, it was found that MyD88 siRNA pretreatment also partially alleviates the oxidative stress injury in the SIC cell model. Conclusion: In sum, our study demonstrated that miR-340-5p can improve myocardial oxidative stress injury by targeting MyD88 in SIC.
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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.