Abstract
Autophagy is responsible for the lysosomal degradation of proteins, organelles, microorganisms and exogenous particles. Epidermis primarily consists of keratinocytes which functions as an extremely important barrier. Investigation on autophagy in keratinocytes has been continuously renewing, but is not so systematic due to the complexity of the autophagy machinery. Here we reviewed recent studies on the autophagy in keratinocyte with a focus on interplay between autophagy machinery and keratinocytes biology, and novel autophagy regulators identified in keratinocytes. In this review, we discussed the roles of autophagy in apoptosis, differentiation, immune response, survival and melanin metabolism, trying to reveal the possible involvement of autophagy in skin aging, skin disorders and skin color formation. Since autophagy routinely plays a double-edged sword role in various conditions, its functions in skin homeostasis and potential application as a therapeutic target for skin diseases remains to be clarified. Furthermore, more investigations are needed on optimizing designed strategies to inhibit or enhance autophagy for clinical efficacy.
Highlights
Two ubiquitin-like conjugation systems of ATG5– ATG12 protein complex and microtubule-associated www.impactjournals.com/oncotarget protein light chain 3 (LC3) are essential for the process of autophagosome formation
As a highly conserved intracellular mechanism for homeostasis maintenance, autophagy is proved to participate in series of physiological activities in keratinocytes, including apoptosis, differentiation, inflammation and melanin metabolism
Autophagy is even closely related to senescence, aging, skin color formation, and displays the ability of anti-stress and anti-infection
Summary
Two ubiquitin-like conjugation systems of ATG5– ATG12 protein complex and microtubule-associated www.impactjournals.com/oncotarget protein light chain 3 (LC3) are essential for the process of autophagosome formation. Several proteins were reported recently to involve in regulation of keratinocyte differentiation targeting on distinct autophagy machinery effectors. The activated TLR2/6 led to an increase of p62 expression and autophagy level, and some components in TLR/NF-κB signal such as myeloid differentiation primary response protein 88 (MyD88) and TNFR-associated factor 6 (TRAF6) were necessary for this induction effect [48].
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