Ultraviolet B radiation down-regulates ULK1 and ATG7 expression and impairs the autophagy response in human keratinocytes

Adiponectin inhibits cardiac arrest/cardiopulmonary resuscitation‑induced apoptosis in brain by increasing autophagy involved in AdipoR1‑AMPK signaling

“…The present study demonstrated that aPn inhibited the activation of aMPK (Ser182) in the brain tissue at the early post-Gcir period (0.5 h) and then enhanced it at 3 and 12 h of reperfusion, accompanied by decreased apoptosis and increased autophagy. although chen et al (26) have demonstrated this hypothesis in keratinocytes in cardiac and liver cells, no previous studies have suggested that aPn activated aMPK (Ser182) signaling pathway to reduce roS induced-apoptosis to autophagy in Gcir injury induced by ca-cPr. Thus, it is concluded that aPn may be involved in the protection of neurons in the brain tissue of post-roSc mice by regulating the activation of aMPK (Ser182), although other studies have reported the priority activation site being Thr172 (44,45).…”

“…However, excessive autophagy also harms the cells, which also results in tissue injury (38). Previous studies have reported that both autophagy and apoptosis are involved in the pathology of cerebral hemorrhage, ischemic stroke and craniocerebral trauma (26)(27)(28). liu et al (39) indicates that arousing autophagy relieves the brain injury by decreasing the apoptotic and necrotic cells.…”

“…chen et al (26) demonstrated that uVB radiation impairs the autophagy response via the phosphorylation of aMPK at the site of Ser182, as well as stimulating reactive oxidative stress in keratinocytes. To determine the effects of Gcir on aMPK activation in brain tissue, the p-aMPK (Ser182)/aMPK ratio was measured.…”

Integrating DNA damage response and autophagy signalling axis in ultraviolet-B induced skin photo-damage: a positive association in protecting cells against genotoxic stress

“…This study demonstrates that UV-B radiation impairs the autophagy response by downregulating several autophagy-related genes in keratinocytes and demonstrates a linkage between autophagy and skin disorders associated with ultraviolet exposure. 36 Other promising studies have found that ATG7 deletion results in increased baseline oxidative stress, reduced ability to degrade cross-linked proteins aer oxidative stress and a strong increase in gH2AX positive nuclei (DNA damage response initiator protein) within the basal layer of Atg7-decient epidermis, suggesting that autophagy deciency signicantly impairs the resistance of the keratinocytes to intrinsic and environmental oxidative stress and results in DNA damage, cell cycle arrest and a disturbed lipid phenotype, which are all typical of a premature cell aging response. 37 Further research in this domain has revealed that anti-aging strategies involving the use of natural plant-based anti-oxidants alleviate the cellular damage to UV-B exposed skin cells by either adjusting the adaptation of cells to stresses or reducing the stress response through improving autophagy levels and thereby restoring cellular homeostasis upon exposure of skin to UV-B.…”

The impact of ultraviolet radiation on skin photoaging — review of in vitro studies

“…In the case of skin aging, the basic level of autophagy increases during the replicable aging of human facial fibroblasts 24 . Furthermore, UVA induce autophagy in fibroblasts 25 and UVB in human keratinocytes 26 . However, the process of autophagy is not capable of completely cancelling out the aging reaction of these cell types and only delaying it 27,28 .…”