ArticleOxidative medicine and cellular longevity2022
The Overexpression of miR-377 Aggravates Sepsis-Induced Myocardial Hypertrophy by Binding to Rcan2 and Mediating CaN Activity.
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 4 papers, 1 of them a synthesis that pooled it.
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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
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.
- MicroRNAs as regulators of cardiac dysfunction in sepsis: pathogenesis and diagnostic potential.Frontiers in cardiovascular medicine · 2025Pooled it
- Wnt-5a ameliorates sepsis-induced downregulation of renal AQP2 via the calcineurin signaling pathway.Clinical and experimental nephrology · 2025Article
- miR-31-5p suppresses myocardial hypertrophy by targeting Nfatc2ip.Journal of cellular and molecular medicine · 2024Article
- miR-29b-1-5p exacerbates myocardial injury induced by sepsis in a mouse model by targeting TERF2.Acta biochimica et biophysica Sinica · 2024Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
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Abstract
Sepsis remains a complicated and incompletely understood syndrome, and myocardial dysfunction is one of the main complications contributing to poor clinical outcomes. Accumulating evidence has revealed the critical involvement of the deregulated expression of specific microRNAs (miRNAs) in cardiac pathologies caused by sepsis. Intriguingly, miR-377 has been correlated with cardiomyocyte apoptosis, whereas its effect on myocardial hypertrophy remains to be illustrated. Thus, the current study sets out to explore the impact and underlying mechanism of miR-377 on myocardial hypertrophy induced by sepsis. The expression pattern of miR-377 was detected in myocardial tissues of septic mice induced by cecal ligation-perforation (CLP). We found that miR-377 was highly expressed in myocardial tissues of CLP-induced septic mice with cardiomyocyte hypertrophy. Besides, miR-377 inhibition could relieve cardiomyocyte hypertrophy and reduce inflammation in septic mice. Further, mechanistic studies found that miR-377 could target Rcan2 and then regulate calcineurin (CaN) activity via Ca
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