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Updated: Feb 13, 2026

Quantitative Visualization and Detection of Skin Cancer Using Dynamic Thermal Imaging
Published on: May 5, 2011
Photoaging and skin cancer: Is the inflammasome the missing link?
Fawaz Awad1, Eman Assrawi1, Camille Louvrier1
1Sorbonne Université, INSERM, UMR_S 933, Assistance Publique Hôpitaux de Paris, Hôpital Trousseau, Département de Génétique médicale, Paris, F-75012, France.
Abstract:
Photoaging and epithelial skin tumorigenesis are complex processes triggered mainly by UV radiation from chronic sun exposure. This leads to DNA damage and reactive oxygen species (ROS) production, which initiate an inflammatory response that alters cell structure and function. Changes in cell homeostasis and ROS production activate intracellular multiprotein platforms called inflammasomes. Inflammasomes nucleate around cytoplasmic receptors mainly of the NLR (nucleotide-binding domain and leucine-rich repeat) family and regulate caspase-1-dependant secretion of pro-inflammatory interleukin (IL)1β and IL18 cytokines, and an inflammatory form of death named pyroptosis. NLRP1 inflammasomes have taken centre stage in skin biology, as mutations in NLRP1 underlie the genetic etiology of dermatological diseases and increase the susceptibility to skin cancer. Targeting inflammasome(s) might be an important approach to improve skin inflammation, photoaging and reduce the risk of epithelial skin tumorigenesis. In this context, we discuss the potential implication of NLRP1 and NLRP3 inflammasomes.
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