ArticleInflammation2021
LncRNA H19 Inhibits the Progression of Sepsis-Induced Myocardial Injury via Regulation of the miR-93-5p/SORBS2 Axis.
Article in Inflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- MicroRNAs as regulators of cardiac dysfunction in sepsis: pathogenesis and diagnostic potential.Frontiers in cardiovascular medicine · 2025Pooled it
- Epigenetic Mechanisms in Sepsis-Induced Cardiomyopathy: From Pathophysiology to Therapeutic Targets.International journal of molecular sciences · 2026Review
- SORBS2: A Molecular Nexus in Multisystem Diseases Through Scaffold-Mediated Regulation.Journal of cellular and molecular medicine · 2026Review
- Neuroepigenetic regulation by long non-coding RNAs in sepsis-associated encephalopathy: cell-type programs and translational biomarkers.Neurogenetics · 2026Review
- Roles of autophagy in sepsis-induced myocardial dysfunction: a comprehensive review.American journal of translational research · 2026Review
- Sevoflurane alleviates hypoxia/reoxygenation-induced myocardial cell injury by regulating miR-93-5p.Toxicology research · 2025Article
- Impact of Sorbs2 dysfunction on cardiovascular diseases.Biochimica et biophysica acta. Molecular basis of disease · 2025Review
- Genome-wide analysis of m6A-modified circRNAs in the mouse model of myocardial injury induced by obstructive sleep apnea.BMC pulmonary medicine · 2025Article
- The role of exosomal lncRNAs in cardiovascular disease: Emerging insights based on molecular mechanisms and therapeutic target level.Non-coding RNA research · 2025Review
- Current Perspectives of Mitochondria in Sepsis-Induced Cardiomyopathy.International journal of molecular sciences · 2024Review
- Role of LncRNAs in the Pathogenesis of Sepsis and their Clinical Significance.Current molecular medicine · 2024Review
- Revealing Landscape of Competing Endogenous RNA Networks in Sepsis-Induced Cardiovascular Diseases.Reviews in cardiovascular medicine · 2023Review
- Protective effect and mechanism of γ-secretase inhibitor on myocardial injury in sepsis rats.American journal of translational research · 2023Article
- Emerging roles of microRNAs in septic cardiomyopathy.Frontiers in pharmacology · 2023Review
- LncRNA H19: a novel player in the regulation of diabetic kidney disease.Frontiers in endocrinology · 2023Review
- LncRNA H19 alleviates sepsis-induced acute lung injury by regulating the miR-107/TGFBR3 axis.BMC pulmonary medicine · 2022Article
- The Interplay of Oxidative Stress and ROS Scavenging: Antioxidants as a Therapeutic Potential in Sepsis.Vaccines · 2022Review
- miR-211-5p Alleviates the Myocardial Ischemia Injury Induced by Ischemic Reperfusion Treatment via Targeting FBXW7.BioMed research international · 2022Article
- Article
- A novel classification based on non-apoptosis cell death predicts clinical outcomes and immunotherapy response of clear renal cell carcinoma.American journal of translational research · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis is an infectious disease that seriously endangers human health. It usually leads to myocardial injury which seriously endangers to the health of human beings. H19 has been confirmed to play key roles in various diseases, including sepsis. However, its function in the progression of sepsis-induced myocardial injury remains largely unknown. H9C2 cells were treated with lipopolysaccharide (LPS) to mimic sepsis-induced myocardial injury in vitro. Cell proliferation and apoptosis were detected by MTT assay and flow cytometry, respectively. In addition, gene and protein expression levels in H9C2 cells were measured by quantitative real-time PCR (qRT-PCR) and Western blotting. The levels of inflammatory cytokines in H9C2 cell supernatants were tested by ELISA. JC-1 staining was performed to observe the mitochondrial membrane potential level in H9C2 cells. H19 and SORBS2 were downregulated in H9C2 cells following LPS treatment, while miR-93-5p was upregulated. Moreover, LPS-induced cell growth inhibition and mitochondrial damage were significantly reversed by overexpression of H19. In addition, H19 upregulation notably suppressed LPS-induced inflammatory responses in H9C2 cells. Moreover, H19 sponged miR-93-5p to promote SORBS2 expression. Overall, H19 suppressed sepsis-induced myocardial injury via regulation of the miR-93-5p/SORBS2 axis. H19 attenuated the development of sepsis-induced myocardial injury in vitro via modulation of the miR-93-5p/SORBS2 axis. Thus, H19 could serve as a potential target for the treatment of sepsis-induced myocardial injury.
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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.