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
Ox-LDL reconfigures the fatty acid metabolism within macrophages and sustains chronic inflammation by upregulating CD36 and its downstream fatty acid transport system (153)
A., Ansari, M
Nothing in the published data licenses treating this molecule as a finished, approved medicine
Investigator Svenja Zielke established a rigorous criterion for autophagy-dependent cell death and carefully identified three effective agents - loperamide, pimozide, and STF-62247 - from a wide range of over 70 compounds that induce autophagy
