ArticleAmerican journal of translational research2020
Inhibition of MyD88 by a novel inhibitor reverses two-thirds of the infarct area in myocardial ischemia and reperfusion injury.
Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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Who cites it
17 citing papers in PubMed.
- Blocking MyD88 Signaling Pathway Protects Against Myocardial Ischemia Reperfusion by Inhibiting NOX/ROS Pathway and Enhancing eNOS Activity.International journal of molecular sciences · 2026Article
- Toll-Like Receptors in the Mechanism of Hexabromocyclododecane-Induced Production of Pro-Inflammatory Cytokines.Journal of applied toxicology : JAT · 2026Article
- The role of toll-like receptors in tributyltin-, dibutyltin-, and pentachlorophenol-induced stimulation of tumor necrosis factor-alpha (TNFα) production in human immune cells.Archives of toxicology · 2026Article
- Review
- Myocardial Ischemia/Reperfusion Injury: Molecular Insights, Forensic Perspectives, and Therapeutic Horizons.Cells · 2025Review
- Attenuation of Pulmonary Fibrosis by the MyD88 Inhibitor TJ-M2010-5 Through Autophagy Induction in Mice.Biomedicines · 2025Article
- Toll-Like Receptors in Pentachlorophenol- and Dibutyltin-Induced Production of Pro-Inflammatory Cytokines, Interleukin (IL)-1β, and IL-6, by Human Immune Cells.Journal of applied toxicology : JAT · 2025Article
- Tissue-resident CCR2Cell reports · 2025Article
- Cardioprotective strategies in myocardial ischemia-reperfusion injury: Implications for improving clinical translation.Journal of molecular and cellular cardiology plus · 2025Review
- Fibroblast-specific MyD88-dependent signaling aggravates inflammation and cardiac dysfunction in the MI heart.Biochimica et biophysica acta. Molecular basis of disease · 2025Article
- MyD88 and Its Inhibitors in Cancer: Prospects and Challenges.Biomolecules · 2024Review
- Innate immune modulation in transplantation: mechanisms, challenges, and opportunities.Frontiers in transplantation · 2023Review
- Circular RNA circ-RCCD promotes cardiomyocyte differentiation in mouse embryo development via recruiting YY1 to the promoter of MyD88.Journal of cellular and molecular medicine · 2022Article
- Blockade of Myd88 signaling by a novel MyD88 inhibitor prevents colitis-associated colorectal cancer development by impairing myeloid-derived suppressor cells.Investigational new drugs · 2022Article
- ST2825, a Small Molecule Inhibitor of MyD88, Suppresses NF-κB Activation and the ROS/NLRP3/Cleaved Caspase-1 Signaling Pathway to Attenuate Lipopolysaccharide-Stimulated Neuroinflammation.Molecules (Basel, Switzerland) · 2022Article
- Immune checkpoint inhibitor therapy increases systemic SDF-1, cardiac DAMPs Fibronectin-EDA, S100/Calgranulin, galectine-3, and NLRP3-MyD88-chemokine pathways.Frontiers in cardiovascular medicine · 2022Article
- TJ-M2010-5, a novel CNS drug candidate, attenuates acute cerebral ischemia-reperfusion injury through the MyD88/NF-κB and ERK pathway.Frontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiomyocytes, macrophages, and fibroblasts play important roles in inflammation and repair during myocardial ischemia/reperfusion injury (MIRI). Myeloid differentiation primary response 88 (MyD88) is upregulated in immunocytes, cardiomyocytes, and fibroblasts during MIRI. MyD88 induces the secretion of proinflammatory cytokines, including interleukin (IL)-1β, IL-6, and tumor necrosis factor alpha (TNF-α), while fibroblasts are recruited and activated to mediate cardiac remodeling. The aim of this study was to assess the anti-MIRI effect and mode of action of the novel MyD88 inhibitor TJ-M2010-5. We synthesized TJ-M2010-5 and identified its target by co-immunoprecipitation, after which we established a murine MIRI model and tested the protective effect of TJ-M2010-5 by immunohistochemistry, flow cytometry, real-time PCR, and western blotting. Neonatal rat cardiomyocytes subjected to anoxia/reoxygenation were also isolated and their supernatants used to stimulate cardiac macrophagocytes and fibroblasts
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Registered trials
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