ArticleThe Journal of international medical research2020
MicroRNA-421 improves ischemia/reperfusion injury via regulation toll-like receptor 4 pathway.
Article in The Journal of international medical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 14 citations in OpenAlex.
- Exosomes-Mediated Signaling Pathway: A New Direction for Treatment of Organ Ischemia-Reperfusion Injury.Biomedicines · 2024Review
- CircRNA Interference Pathway: A New Target for Intervention in Different Stages of Heart Failure.Current topics in medicinal chemistry · 2024Review
- LncRNA small nucleolar RNA host gene 16 reduces sepsis-induced myocardial damage by regulating miR-421/suppressor of cytokine signaling 5 axis.The Kaohsiung journal of medical sciences · 2022Article
- Signaling pathways and targeted therapy for myocardial infarction.Signal transduction and targeted therapy · 2022Review
- The crosstalk between STAT3 and microRNA in cardiac diseases and protection.Frontiers in cardiovascular medicine · 2022Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesThe objective was to investigate the effects of microRNA-421 against myocardial ischemia/reperfusion injury in C57BL/6 mice.
methodsMale C57BL/6 mice (n = 27) were randomly divided into three groups: normal control (NC) group (sham-treated); I/R model group, which underwent the I
resultsCompared with the NC group, in the model group, the myocardial infarction was large; inflammatory cell infiltration was severe; apoptosis was enhanced; expression of TLR4, JAK2, and STAT3 was increased; and serum concentrations of IL-6, TNF-α, IL-10, and HMGB1 were significantly increased. In the miRNA group, the ischemia/reperfusion injury was significantly improved.
conclusionsOverexpression of miRNA-421 could reduce ischemia/reperfusion inflammatory response, perhaps via inactivation of TLR4, JAK2, and STAT3.
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Registered trials
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