Toll-like receptor 7 constrains efferocytosis in myocardial injury - PubMed
3 days ago
- #Efferocytosis
- #TLR7
- #Myocardial Injury
- TLR7 deficiency reduces inflammation, infarct size, and adverse remodeling in myocardial ischemia-reperfusion injury.
- TLR7 deficiency reprograms macrophages toward a reparative phenotype with increased anti-inflammatory mediators like IL-10 and TGF-β.
- Single-cell RNA sequencing shows TLR7 deficiency suppresses inflammatory signaling in M1 macrophages and enhances efferocytosis pathways in M2 macrophages.
- TLR7 deficiency upregulates phagocytic receptors (CD36, LRP1, MerTK, AXL, Rac1), boosting efferocytosis and reducing apoptotic burden.
- TLR7 deficiency promotes clearance of neutrophil extracellular traps (NETs) without affecting NETosis, aiding inflammation resolution.
- NET formation occurs in myocardial injury models and patients after percutaneous coronary intervention.
- TLR7 acts as a macrophage-intrinsic checkpoint limiting efferocytosis and NET disposal, impairing post-injury inflammation resolution.
- Targeting TLR7 may be therapeutic to suppress excessive inflammation and restore pro-resolving macrophage functions for cardiac repair.