ArticleInflammation2019
Attenuation of Sepsis-Induced Cardiomyopathy by Regulation of MicroRNA-23b Is Mediated Through Targeting of MyD88-Mediated NF-κB Activation.
Article in Inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 3 of them syntheses that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 3 syntheses or guidelines pooled it, 41 citations in OpenAlex.
- MicroRNAs as regulators of cardiac dysfunction in sepsis: pathogenesis and diagnostic potential.Frontiers in cardiovascular medicine · 2025Pooled it
- Expression of MicroRNAs in Sepsis-Related Organ Dysfunction: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- MicroRNAs and Sepsis-Induced Cardiac Dysfunction: A Systematic Review.International journal of molecular sciences · 2020Pooled it
- Fucoidan: An Update on Function, Role in Human Health and Applications.Chemical biology & drug design · 2026Review
- Development and Validation of Early Alert Model for Diabetes Mellitus-Tuberculosis Comorbidity.Microorganisms · 2025Article
- Therapeutic effects of platelet-derived extracellular vesicles on viral myocarditis correlate with biomolecular content.Frontiers in immunology · 2024Article
- MiR-146b-5p enriched bioinspired exosomes derived from fucoidan-directed induction mesenchymal stem cells protect chondrocytes in osteoarthritis by targeting TRAF6.Journal of nanobiotechnology · 2023Article
- Reconstituted Extracellular Vesicles from Human Platelets Decrease Viral Myocarditis in Mice.Small (Weinheim an der Bergstrasse, Germany) · 2023Article
- Xinyang tablet ameliorates sepsis-induced myocardial dysfunction by regulating Beclin-1 to mediate macrophage autophagy and M2 polarization through LncSICRNT1 targeting E3 ubiquitin ligase TRAF6.Chinese medicine · 2023Article
- Emerging roles of microRNAs in septic cardiomyopathy.Frontiers in pharmacology · 2023Review
- Long non-coding RNA Sox2OT promotes coronary microembolization-induced myocardial injury by mediating pyroptosis.ESC heart failure · 2022Article
- Research Progress on the Mechanism of Sepsis Induced Myocardial Injury.Journal of inflammation research · 2022Review
- MicroRNAs Promote the Progression of Sepsis-Induced Cardiomyopathy and Neurovascular Dysfunction Through Upregulation of NF-kappaB Signaling Pathway-Associated HDAC7/ACTN4.Frontiers in neurology · 2022Article
- MiR-539-5p inhibits the inflammatory injury in septic H9c2 cells by regulating IRAK3.Molecular biology reports · 2022Article
- The mechanism of sevoflurane post-treatment alleviating hypoxic-ischemic encephalopathy by affecting histone methyltransferase G9a in rats.Bioengineered · 2021Article
- Predictive value and regulatory mechanism of serum miR-499a-5p on myocardial dysfunction in sepsis.Journal of cardiothoracic surgery · 2021Article
- Protective Effect of Sirtuin 3 on CLP-Induced Endothelial Dysfunction of Early Sepsis by Inhibiting NF-κB and NLRP3 Signaling Pathways.Inflammation · 2021Article
- Inhibition of miR‑101‑3p protects against sepsis‑induced myocardial injury by inhibiting MAPK and NF‑κB pathway activation via the upregulation of DUSP1.International journal of molecular medicine · 2021Article
- Down-regulation of lncRNA CASC9 aggravates sepsis-induced acute lung injury by regulating miR-195-5p/PDK4 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Article
- LncRNA KCNQ1OT1 attenuates sepsis-induced myocardial injury via regulating miR-192-5p/XIAP axis.Experimental biology and medicine (Maywood, N.J.) · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Myocardial cell injury or cardiomyopathy is associated with excessive inflammatory response and apoptosis of cardiac myocytes during sepsis. MicroRNA-23b (miR-23b) is a multifunctional miRNA that is considered to regulate immunosuppression in sepsis. The aim of this study was to examine the effect of miR-23b on cardiomyopathy induced by sepsis and to explore the potential mechanism involved. Sprague-Dawley rats were subjected to cecal ligation and puncture (CLP), and the level of miR-23b at different time points was measured by quantitative real-time polymerase chain reaction (qPCR). Then, we overexpressed miR-23b in vivo and in vitro. The rats were subjected to CLP 7 days after transfection. Cardiac function, inflammatory response, and heart tissues were examined 3 days thereafter. In an in vitro experiment, H9C2 cardiomyoblasts were stimulated with lipopolysaccharide (LPS) after transfection of miR-23b, following which apoptosis and the level of NF-κB were analyzed. The expression of miR-23b was upregulated during polymicrobial sepsis, and transfection of miR-23b lentivirus improved the outcome of sepsis-induced cardiomyopathy by attenuating inflammatory responses and protecting against histopathological damage. In in vitro experiments, elevated miR-23b inhibited excessive apoptosis of cardiomyocytes, which may be because activation of the NF-κB signaling pathway was inhibited by the decreased levels of TRAF6 and IKKβ. Therefore, miR-23b improved sepsis-induced cardiomyopathy by attenuating the inflammatory response, suppressing apoptosis, and preventing NF-κB activation via targeted inhibition of TRAF6 and IκκB. These results indicated that miR-23b may represent a novel therapeutic approach for clinical treatment of sepsis-induced cardiomyopathy.
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Registered trials
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.