ArticleCellular & molecular biology letters2020
Inhibition of microRNA-15 protects H9c2 cells against CVB3-induced myocardial injury by targeting NLRX1 to regulate the NLRP3 inflammasome.
Article in Cellular & molecular biology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- NLRX1 emerges as the only observed essential regulator of the mPTP, challenging mPTP inhibition as a valid target of cardioprotection.Basic research in cardiology · 2026Review
- Ubiquitination-mediated degradation of NLRX1 drives metabolic vulnerability and accelerates intervertebral disc degeneration.Cell death and differentiation · 2026Article
- Macrophage USP7 aggravates acute myocardial infarction by inhibiting STING degradation through the ESCRT pathway.Cell death and differentiation · 2026Article
- Exploring the mechanism of saffron in treating viral myocarditis using network pharmacology and molecular docking.Medicine · 2026Article
- NLRX1 alleviates sepsis-induced acute lung injury by activating mitophagy and suppressing NLRP3 inflammasome activation.Frontiers in pharmacology · 2026Article
- Review
- Determining the biomarkers and pathogenesis of myocardial infarction combined with ankylosing spondylitis via a systems biology approach.Frontiers of medicine · 2025Article
- Regulatory role of microRNAs in virus-mediated inflammation.Journal of inflammation (London, England) · 2024Review
- MINOCA: A Pathophysiological Approach of Diagnosis and Treatment-A Narrative Review.Biomedicines · 2024Review
- The Role of MicroRNA in the Pathophysiology and Diagnosis of Viral Myocarditis.International journal of molecular sciences · 2024Review
- NLRP4E regulates actin cap formation through SRC and CDC42 during oocyte meiosis.Cellular & molecular biology letters · 2024Article
- miR-29b-3p regulates cardiomyocytes pyroptosis in CVB3-induced myocarditis through targeting DNMT3A.Cellular & molecular biology letters · 2024Article
- A Narrative Review of Preclinical In Vitro Studies Investigating microRNAs in Myocarditis.Current issues in molecular biology · 2024Review
- High-Density Lipoproteins at the Interface between the NLRP3 Inflammasome and Myocardial Infarction.International journal of molecular sciences · 2024Review
- Macrophage-driven cardiac inflammation and healing: insights from homeostasis and myocardial infarction.Cellular & molecular biology letters · 2023Review
- Roles of inflammasomes in viral myocarditis.Frontiers in cellular and infection microbiology · 2023Review
- The role of non-coding RNAs in myocarditis: a narrative review.Annals of translational medicine · 2022Review
- Cardiomyocyte death in sepsis: Mechanisms and regulation (Review).Molecular medicine reports · 2022Review
- Luteolin Protects Cardiomyocytes Cells against Lipopolysaccharide-Induced Apoptosis and Inflammatory Damage by Modulating Nlrp3.Yonsei medical journal · 2022Article
- The roles of Eph receptors, neuropilin-1, P2X7, and CD147 in COVID-19-associated neurodegenerative diseases: inflammasome and JaK inhibitors as potential promising therapies.Cellular & molecular biology letters · 2022Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundViral myocarditis (VMC) is a type of cardiac inflammation that is generally caused by coxsackievirus B3 (CVB3) infection. Several MicroRNAs (miRNAs) are known to play crucial roles in VMC pathogenesis. MiR-15 is reportedly associated with myocardial injury, inflammatory responses and viral infection. Whether miR-15 affects the occurrence and development of VMC remains largely unknown. The roles of miR-15 and their underlying mechanisms in CVB3-stimulated H9c2 cells were assessed in this study.
methodsWe infected H9c2 cells with CVB3 to establish a VMC cellular model. We then determined the effects of miR-15 inhibition on three cardiomyocyte injury markers: lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB) and cardiac troponin-I (cTn-I). The impact on CVB3-induced cell apoptosis and pro-inflammatory cytokines was also investigated. The effects of miR-15 inhibition on NLRP3 inflammasome activation were also assessed. The target relationship between miR-15 and NOD-like receptor X1 (NLRX1) was determined using a luciferase reporter assay.
resultsMiR-15 expression was significantly upregulated in H9c2 cells after CVB3 infection. Inhibition of miR-15 significantly decreased the CVB3-induced levels of LDH, CK-MB and cTn-I. It also elevated cell viability, reduced CVB3-induced cell apoptosis and decreased the generation of the interleukins IL-1β, IL-6 and IL-18. Furthermore, we determined that miR-15 inhibition suppressed NLRP3 inflammasome activation by downregulating NLRP3 and caspase-1 p20 expression. We found a direct target relationship between miR-15 and NLRX1. Additionally, inhibition of NLRX1 reversed the protective effects of miR-15 inhibition against CVB3-induced myocardial cell injury by regulating the NLRP3 inflammasome.
conclusionOur results indicate that miR-15 inhibition alleviates CVB3-induced myocardial inflammation and cell injury. This may be partially due to NLRX1-mediated NLRP3 inflammasome inactivation.
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