Photoaging and skin cancer: Is the inflammasome the missing link?

Date
2018-03-12
Authors
Awad, Fawaz
Assrawi, Eman
Louvrier, Camille
Jumeau, Claire
Giurgea, Irina
Journal Title
Journal ISSN
Volume Title
Publisher
Elsevier
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.
Description
Keywords
NLRP1, NLRP3, Inflammasome, Keratinocytes, Cytokines, Skin cancer
Citation