Facial aging

Skin aging is influenced by intrinsic and extrinsic factors, such as sun exposure. This leads to changes in the epidermis and dermis, causing wrinkles and other signs of aging. Extracellular matrix integrity and hydration are essential for skin health.

The skin and underlying bone and cartilage structures, as well as adipose tissue and muscles, age chronologically and biologically. Aging is determined by intrinsic and extrinsic factors, such as declining hormone levels, reduced repair capacity of deoxyribonucleic acid (DNA), accumulation of DNA mutations caused by DNA radicals and the accumulation of DNA mutations.These include intrinsic and extrinsic factors, such as decreased hormone levels, reduced DNA repair capacity, accumulation of DNA mutations caused by free radicals or ultraviolet (UV) radiation, and additional environmental factors, such as air pollution, malnutrition and smoking.

Among these environmental factors, UV radiation contributes up to 80%. UV-induced skin aging or photoaging is defined as the premature appearance of signs of aging in the skin, and presents with characteristic morphological changes of the epidermal and dermal compartments.

Skin aging occurs at different levels in the epidermis, dermis and dermoepidermal junction. The skin provides barrier functions, wound healing, thermoregulation, sensory function, immune function and vitamin D metabolism, which globally decrease with increasing age. Alterations in skin structure result in skin laxity, wrinkles, sagging and skin neoplasms.

The structural stability of the epidermis, dermis and hypodermis depends on the integrity of the extracellular matrix, such as collagen and elastin, a stable cell proliferation process, intact vascularization and sufficient barrier function with lipids and skin hydration.

The biological age of the skin can be analyzed by skin structure, including thickness, collagen matrix and cell size, as well as by functional analysis with lipid and hydration measurements.functional analysis with measurements of elasticity, torsional extensibility, neuroperception, transepidermal water loss (TEWL) and proliferation rate.

Number of observed variants

13.5 million variants

Number of risk loci

55 loci

Genes analyzed

AKAP1 AKAP12 ARAP2 ARL15 AXIN2 BNC2 BRD1 CDC42EP3 CHRNA5 CYP11A1 DOCK8 EFEMP1 EIF2B2 EIF2S2 ELN EXOSC6 FADS2 FLACC1 FMN1 GSDMC IRF4 JAZF1 JMJD1C KLHL6 LHX8 LOXL1 LYPLAL1 MAP3K1 MEMO1 MFAP4 MKLN1 NDUFS3 NDUFS4 NFIC NICN1 P4HA2 PAX1 PAX3 PCDH9 PLCG1 PLXNA1 RAD52 RNLS ROGDI RXFP3 SEMA4D SLC39A8 SLC45A1 SRPK2 SUPT3H SYNE2 TRPS1 TUBB3 TWIST2 WNT10A ZBTB20 ZEB2

Bibliography

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