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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.

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Endothelial Dysfunction in Vascular Inflammation: The Role of NLRP3, NLRP10, AIM2, TLR9, and PANoptosis

  • 章节

  • 发表日期：

    2026年

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  • Diana L. Silva-Velasco,
  • Rinaldo R. Dos Passos,
  • Raiana Anjos Moraes,
  • Tiago Tomazini Gonçalves,
  • Stephanie Wilczynski,
  • Tianxin Zhang,
  • Stephanie Randar,
  • Jeremiah Tobin,
  • Mark J. Uline,
  • Fernanda Priviero,
  • R. Clinton Webb

摘要

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.