ArticleBiochimica et biophysica acta. Molecular basis of disease2025
Fibroblast-specific MyD88-dependent signaling aggravates inflammation and cardiac dysfunction in the MI heart.
Article in Biochimica et biophysica acta. Molecular basis of disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Inhibition of MyD88 in Tubular Epithelial Cells Alleviates the Cellular Senescence in Sepsis-Associated Acute Kidney Injury.Inflammation · 2026Article
- RNA 5-Methylcytosine Modification in Myocardial Fibrosis.Reviews in cardiovascular medicine · 2025Review
- Myeloid MyD88 Mediates Macrophage Infiltration and Activation in Ang II-Induced Cardiac Hypertrophy.Journal of cellular and molecular medicine · 2025Article
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8 authors.
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Abstract
backgroundExcessive fibrosis and chronic inflammation are vital to adverse cardiac remodeling of the MI heart. The crosstalk of fibroblasts (FBs) (primary drivers of fibrosis) and immune cells (that govern inflammation) is critical for the repair and remodeling of the injured heart. However, the molecular mechanisms through which FBs communicate with immune cells are poorly understood. In the MI heart, substantial cardiac cell damage releases alarmins, which trigger an immune response through the TLR/MyD88 pathway. The role of MyD88-dependent signaling is well characterized in immune cell biology. However, the role of FB-derived MyD88 signaling in MI heart injury is unknown.
objectiveTo define the role of FB-MyD88 in MI pathology. METHODS AND
resultsMyD88 was deleted from fibroblasts or myofibroblasts with tamoxifen-inducible Tcf21- or Postn- promoter-driven Cre recombinase. Control and MyD88 KO mice were subjected to permanent LAD ligation (MI injury), and cardiac parameters were evaluated. Additionally, co-culture experiments and chemokine profiling were conducted to identify mechanisms facilitating FB-immune cell crosstalk. FB-specific MyD88 deletion restricted MI-induced adverse cardiac remodeling and cardiac dysfunction. Surprisingly, FB-specific MyD88 deletion reduced myeloid cell recruitment and molecular markers of chronic inflammation in the KO heart. The mechanistic studies confirmed that MyD88 is required for the activation of NF-κB in FBs. Additionally, co-culture experiments demonstrated that FB-MyD88 facilitates immune cell crosstalk through chemokines and promotes an inflammatory gene program.
conclusionThese findings suggest that FB-MyD88 promotes MI-induced chronic inflammation and cardiac dysfunction. Therefore, targeting MyD88 could serve as a potential therapeutic strategy.
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