Macrophage-derived galectin-3 contributes to pyroptosis, apoptosis and necroptosis through TLR4/MyD88/NF-κB/NLRP3 during atherosclerosis - PubMed
5 days ago
- #galectin-3
- #PANoptosis
- #atherosclerosis
- Macrophage-derived galectin-3 contributes to pyroptosis, apoptosis, and necroptosis (PANoptosis) in atherosclerosis via the TLR4/MyD88/NF-κB/NLRP3 pathway.
- Galectin-3 and NLRP3 expression levels are elevated in human and murine atherosclerotic lesions, predominantly in macrophages.
- Ox-LDL induces PANoptosis in macrophages, activating NLRP3/GSDMD/CASP3/CASP8/RIPK3/pMLKL and proinflammatory cytokines.
- Galectin-3 interacts with NLRP3; its knockdown reduces inflammatory cell death, while NLRP3 agonist nigericin exacerbates it.
- Genetic galectin-3 deficiency attenuates macrophage death, vascular inflammation, and atherosclerosis in HFD-fed ApoE-/- mice.
- Galectin-3 activates the TLR4/MyD88/NF-κB/NLRP3 axis, promoting PANoptosis-like cell death and atherosclerosis progression.