Autophagy protects from photoageing in skin fibroblasts

Abstract

when conditioning on known susceptibility SNPs in the region. 4 The picture is unclear for the well-known LCE3B/C deletion. This SV is believed to have a mechanistic role in psoriasis, 5,6 a conclusion supported by only two of the three cohorts in which conditional analysis with local SNPs could be performed. 4 The major histocompatibility complex (MHC) harbours multiple independent associations with psoriasis, the primary signal mapping to the HLA-C*06:02 allele. 7 Zhen et al. identify two novel deletions close to HLA-C. 4 Conditional analysis suggests that each contributes independently of HLA-C*06:02 to psoriasis risk, and both are associated with increased expression of HLA-C, highlighting a possible disease mechanism.What is striking is that by appraising SVs the study does not identify novel psoriasis susceptibility loci. But this is unsurprising because most SVs will exhibit some degree of linkage disequilibrium with SNPs already assessed via GWAS. Intriguingly, Zhen et al. find no association with copy number or the common inversion at the b-defensin gene cluster. This locus has been associated with psoriasis susceptibility in a candidate gene study, 8 but never implicated by a large-scale GWAS (as it has for severe acne 9 ).Zhen et al. have presented a systematic and comprehensive investigation, whose primary value is to propose alternative causal genetic variation at psoriasis susceptibility loci. As ever with genetic research, the challenge now is to do this bigger and better. A much larger reference SV map is now available from the Genome Aggregation Database. 1 Larger case-control datasets that utilize genome-wide genotyping data will increase power to detect psoriasis-associated SVs, and data from multiple ethnicities should help pinpoint causal signals, especially in the complex MHC region. More formalized fine-mapping approaches would then also be warranted. 10 A clearer picture of SV-mediated psoriasis risk should be readily achievable as we move into the era of biobank-scale genetics.

Low‐energy green light alleviates senescence‐like phenotypes in a cell model of photoaging

“…Therefore, many targets of photoaging therapy are hypothesized to play a role by acting on dermal fibroblasts, including intense pulsed light 5 . Although the specific mechanism of action is unclear, the change of cellular autophagy may be one of the mechanisms by which light plays its biological role 6 …”

“…5 Although the specific mechanism of action is unclear, the change of cellular autophagy may be one of the mechanisms by which light plays its biological role. 6 …”

“…5 Although the specific mechanism of action is unclear, the change of cellular autophagy may be one of the mechanisms by which light plays its biological role. 6 Autophagy is an important biological process to maintain cell homeostasis. 7 Studies have shown autophagy contributes to UVinduced skin light injury.…”