ArticleAmerican journal of physiology. Cell physiology2025
Contribution of NLRP3-GSDMD axis to PDGF-BB-induced vascular smooth muscle cell phenotypic transition.
Article in American journal of physiology. Cell physiology, 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.
- Targeting integrated cell death networks in sepsis‑associated acute kidney injury: Shared regulatory nodes and diet‑related small molecule modulation (Review).International journal of molecular medicine · 2026Review
- Vascular smooth muscle-specific NLRP3 hyperactivation exacerbates arterial intimal hyperplasia in mice.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Vascular Smooth Muscle-Specific NLRP3 Hyperactivation Drives Arterial Intimal Hyperplasia in Mice.Research square · 2026Article
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13 authors.
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Abstract
Intimal hyperplasia, a pathological form of vascular remodeling, is a hallmark of several cardiovascular diseases, including restenosis following angioplasty. Vascular smooth muscle cell (VSMC) phenotypic transition plays a critical role in the development of vascular intimal hyperplasia. This study investigates the role of the NOD-like receptor pyrin domain 3 (NLRP3) inflammasome and its downstream effector, gasdermin D (GSDMD), in regulating VSMC phenotypic transition and their implications in the development of intimal hyperplasia. In primary cultured VSMCs, platelet-derived growth factor BB (PDGF-BB) stimulated activation of the NLRP3-GSDMD axis, promoting inflammation, proliferation, and migration. Pharmacological inhibition of the inflammasome with the caspase-1 inhibitor YVAD significantly attenuated PDGF-BB-induced GSDMD activation and lactate dehydrogenase release. Furthermore, silencing the
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