ArticleResearch square2026
Vascular Smooth Muscle-Specific NLRP3 Hyperactivation Drives Arterial Intimal Hyperplasia in Mice.
Article in Research square, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
9 authors.
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Abstract
Intimal hyperplasia is a major contributor to restenosis after vascular interventions and to atherosclerotic lesion progression, driven largely by vascular smooth muscle cell (VSMC) inflammatory activation, phenotypic switching, and maladaptive remodeling. While NOD-like receptor pyrin domain 3 (NLRP3) inflammasome activity has been linked to vascular diseases, direct evidence that VSMC-intrinsic NLRP3 hyperactivation drives VSMC dysfunction and intimal hyperplasia in vivo has been lacking. Here, we generated a VSMC-specific
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