The faster reaction with GSSG might reflect the simultaneous interaction of the substrate with both glutathione interaction sites
conversely, inactivation of mTORC1 can induce apoptosis by promoting autophagy
PLoS One 12(4):e0175796 Karmi O, Marjault HB, Pesce L, Carloni P, Onuchic JN, Jennings PA, Mittler R, Nechushtai R (2018) The unique fold and lability of the [2Fe-2S] clusters of NEET proteins mediate their key functions in health and disease
Molecular mechanisms of cutaneous ageing To interpret the effects of dermatological peptides, the molecular alterations of cutaneous ageing must be understood: Intrinsic ageing (chronological) Decreased collagen synthesis by fibroblasts (1% per year after 30) AGE accumulation (Advanced Glycation End-products) by non-enzymatic glycation Fibroblastic senescence with SASP (Senescence-Associated Secretory Phenotype), chronic pro-inflammatory secretion Dermal atrophy , reduced vascularisation, loss of subcutaneous adipocytes Extrinsic ageing (photoageing) UV-B damage : cyclobutane pyrimidine dimers, keratinocyte DNA alteration UV-A and oxidative stress : ROS, lipid peroxidation, protein carbonylation MMP overexpression (MMP-1, MMP-3, MMP-9) via AP-1 activation, degrading collagen and elastin Solar elastosis : accumulation of degraded and dystrophic elastin in the dermis Dermatological peptides act at different levels of these cascades: anabolic stimulation (GHK-Cu, Matrixyl), catabolic inhibition (MMP modulation), anti-oxidant protection (GHK-Cu), inflammatory signalling modulation
More invasive procedures can be used for patients with moderate-to-severe symptoms of BPH, particularly for patients who have not responded to pharmacologic therapy (McVary 2011)
