Handb Exp Pharmacol. 2026 May 26. doi: 10.1007/164_2026_802. Online ahead of print.
ABSTRACT
Endothelial dysfunction is a hallmark of vascular inflammation and a critical step in the development of cardiovascular diseases. Recent evidence highlights the role of inflammasome factors in the inflammatory and cell death pathways that compromise endothelial homeostasis. NLRP3 and AIM2 inflammasomes drive the release of IL-1β and IL-18, amplifying vascular inflammation, while TLR9 responds to mitochondrial DNA to further potentiate endothelial secretion of inflammatory cytokines. In contrast, NLRP10 appears to act as a modulator of inflammasome activity and NF-κB signaling. Together, these sensors converge on processes such as pyroptosis, apoptosis, and necroptosis, which can integrate into PANoptosis, thereby exacerbating endothelial injury. Understanding these mechanisms offers new insights into the interplay between innate immunity and vascular dysfunction, with potential implications for therapeutic interventions.
PMID:42185668 | DOI:10.1007/164_2026_802