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

Publication date: Available online 12 March 2018 Source:Mechanisms of Ageing and Development Author(s): Fawaz Awad, Eman Assrawi, Camille Louvrier, Claire Jumeau, Irina Giurgea, Serge Amselem, Sonia-Athina Karabina 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 IL-18 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.
Source: Mechanisms of Ageing and Development - Category: Geriatrics Source Type: research