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

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dc.contributor.authorAwad, Fawaz
dc.contributor.authorAssrawi, Eman
dc.contributor.authorLouvrier, Camille
dc.contributor.authorJumeau, Claire
dc.contributor.authorGiurgea, Irina
dc.date.accessioned2019-12-18T12:26:21Z
dc.date.available2019-12-18T12:26:21Z
dc.date.issued2018-03-12
dc.description.abstractPhotoaging 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.en_US
dc.identifier.issn0047-6374
dc.identifier.urihttps://dspace.alquds.edu/handle/20.500.12213/5045
dc.language.isoenen_US
dc.publisherElsevieren_US
dc.subjectNLRP1en_US
dc.subjectNLRP3en_US
dc.subjectInflammasomeen_US
dc.subjectKeratinocytesen_US
dc.subjectCytokinesen_US
dc.subjectSkin canceren_US
dc.titlePhotoaging and skin cancer: Is the inflammasome the missing link?en_US
dc.typeArticleen_US
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