Key result
Cigarette tar promotes plaque erosion and endothelial pyroptosis via mitochondrial fission and mtDNA release.
Why the study?
Does cigarette tar induce endothelial cell pyroptosis and plaque erosion in preclinical models?
Does cigarette tar induce endothelial cell pyroptosis and plaque erosion in preclinical models?
Answers are grounded in this paper and cite their sources.
Cigarette tar induces endothelial cell pyroptosis and plaque erosion via CAMKII/Drp1/mtDNA signaling, identifying a potential mechanistic target for reducing plaque erosion.
Smoking is the only cardiovascular risk factor for plaque erosion. We found cigarette tar resulted in erosion-like lesion development in apolipoprotein E-/- mice, with mural thrombosis, discontinuous endothelium, platelet activation, smooth muscle cell proliferation, and hyaluronic acid accumulation in the aorta. Single-cell transcriptomics revealed that genes relating to pyroptosis, platelet activation, and leukocytes adhesion were significantly increased in an endothelial cell subset. Rescue assays indicated cigarette tar caused human coronary artery endothelial cell pyroptosis by enhanced calcium-calmodulin-dependent protein kinase II / dynamin-related protein 1-mediated mitochondrial fission and mitochondrial DNA release via activating Ca2+ signaling. Inhibition of endothelial cell pyroptosis may be a novel therapeutic strategy to reduce plaque erosion.
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Luo et al. (2025) studied Plaque erosion. Cigarette tar was evaluated on Erosion-like lesion development and endothelial cell pyroptosis. Cigarette tar induced erosion-like lesion development and endothelial cell pyroptosis via enhanced CAMKII/Drp1-mediated mitochondrial fission and mtDNA release.
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