ArticleJournal of molecular and cellular cardiology2012
MyD88 mediated inflammatory signaling leads to CaMKII oxidation, cardiac hypertrophy and death after myocardial infarction.
Article in Journal of molecular and cellular cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 146 citations in OpenAlex.
- Signal Recognition Granule Receptor Beta Subunit Promotes Arrhythmogenic Remodeling in the Heart Failure Mice.Journal of the American Heart Association · 2026Article
- Attenuating effects of inflammatory pathway by prolonged left ventricular unloading after myocardial infarction in male rats.PloS one · 2026Article
- Fibroblast-specific MyD88-dependent signaling aggravates inflammation and cardiac dysfunction in the MI heart.Biochimica et biophysica acta. Molecular basis of disease · 2025Article
- The gut microbiota-inflammation-HFpEF axis: deciphering the role of gut microbiota dysregulation in the pathogenesis and management of HFpEF.Frontiers in cellular and infection microbiology · 2025Review
- Macrophage Membrane-Coated Nanocarriers in Myocardial Infarction: A Paradigm Shift in Targeted Cardiac Therapy.International journal of nanomedicine · 2025Review
- Jaranol: a compound with therapeutic activity against pathological cardiac remodelling via multi-target inhibition of the Snai3/TLR2 and NF-κB signaling pathways.Frontiers in pharmacology · 2025Article
- The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration.Nature cardiovascular research · 2024Article
- Sweroside alleviates pressure overload-induced heart failure through targeting CaMKⅡδ to inhibit ROS-mediated NF-κB/NLRP3 in cardiomyocytes.Redox biology · 2024Article
- Leveraging a neutrophil-derived PCD signature to predict and stratify patients with acute myocardial infarction: from AI prediction to biological interpretation.Journal of translational medicine · 2024Article
- Repair of the Infarcted Heart: Cellular Effectors, Molecular Mechanisms and Therapeutic Opportunities.Circulation research · 2024Review
- Calmodulin Contributes to Lipolysis and Inflammatory Responses in Clinical Ketosis Cows through the TLR4/IKK/NF-κB Pathway.Animals : an open access journal from MDPI · 2024Article
- Unveiling the role of CaMKII in retinal degeneration: from biological mechanism to therapeutic strategies.Cell & bioscience · 2024Review
- Role of CaMKII in diabetes induced vascular injury and its interaction with anti-diabetes therapy.Reviews in endocrine & metabolic disorders · 2024Review
- Targeting gut microbiota in aging-related cardiovascular dysfunction: focus on the mechanisms.Gut microbes · 2023Review
- Sotagliflozin attenuates cardiac dysfunction and remodeling in myocardial infarction rats.Heliyon · 2023Article
- The interplay of inflammation, exosomes and CaCardiovascular diabetology · 2023Review
- CaMKII as a Therapeutic Target in Cardiovascular Disease.Annual review of pharmacology and toxicology · 2023Review
- Thalidomide Alleviates Apoptosis, Oxidative Damage and Inflammation Induced by Pemphigus Vulgaris IgG in HaCat Cells and Neonatal Mice Through MyD88.Drug design, development and therapy · 2023Article
- Dysregulated lncRNAs are involved in the progress of myocardial infarction by constructing regulatory networks.Open medicine (Warsaw, Poland) · 2023Article
- Toll-like receptors in cardiac hypertrophy.Frontiers in cardiovascular medicine · 2023Review
21 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The toll-like receptors (TLR) and myocardial infarction (MI) promote NF-κB-dependent inflammatory transcription and oxidative injury in myocardium. The multifunctional Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is activated by oxidation and contributes to NF-κB-dependent transcription, myocardial hypertrophy and post-MI death. The myeloid differentiation protein 88 (MyD88) is an adapter protein critical for many TLR functions, but downstream targets for TLR/MyD88 signaling in MI are not well understood. We asked if CaMKII and TLR/MyD88 pathways are interconnected and if TLR/MyD88 contributes to adverse outcomes after MI. Here we show that TLR-4 activation by lipopolysaccharide (LPS) induces CaMKII oxidation (ox-CaMKII) in cardiomyocytes. MI enhances ox-CaMKII in wild type (WT) hearts but not in MyD88(-/-) hearts that are defective in MyD88-dependent TLR signaling. In post-MI WT hearts expression of pro-inflammatory genes TNF-α (Tnfa), complement factor B (Cfb), myocyte death and fibrosis were significantly increased, but increases were significantly less in MyD88(-/-) hearts after MI. MyD88(-/-) cardiomyocytes were defective in NF-κB activation by LPS but not by the MyD88-independent TLR agonist poly(I:C). In contrast, TNF-α induced Cfb gene expression was not deficient in MyD88(-/-) cardiomyocytes. Several hypertrophy marker genes were upregulated in both WT and MyD88(-/-) hearts after MI, but Acta1 was significantly attenuated in MyD88(-/-) hearts, suggesting that MyD88 selectively affects expression of hypertrophic genes. Post-MI cardiac hypertrophy, inflammation, apoptosis, ox-CaMKII expression and mortality were significantly reduced in MyD88(-/-) compared to WT littermates. These data suggest that MyD88 contributes to CaMKII oxidation and is important for adverse hypertrophic and inflammatory responses to LPS and MI.
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Registered trials
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