Senomorphic activity of a combination of niacinamide and hyaluronic acid: correlation with clinical improvement of skin aging.

Intrinsic and extrinsic factors, including lifestyle and sun exposure, can contribute to cell senescence, which impairs skin homeostasis, that may in turn lead to skin aging. Senescent cells have a specific secretome, called the senescence-associated secretory phenotype (SASP) that includes MMPs, CXCLs and S100A8/9. Reducing the SASP with senotherapeutics is a promising strategy to reduce skin aging. Here we evaluated the effect of a formula containing niacinamide and hyaluronic acid, which are known to limit senescence and skin aging. We conducted three different studies. (1) Ex vivo explants treated with the formula had more collagen and glycosaminoglycan. (2) In a clinical trial with forty-four women, two months of treatment improved fine lines, wrinkles, luminosity, smoothness, homogeneity, and plumpness. (3) In a third study on thirty women, we treated one arm for two months and took skin biopsies to study gene expression. 101 mRNAs and 13 miRNAs were differentially expressed. We observed a likely senomorphic effect, as there was a decrease in many SASP genes including MMP12 and CXCL9 and a significant downregulation of autocrine signaling genes: S100A8 and S100A9. These pharmaco-clinical results are the first to demonstrate the senomorphic properties of an effective anti-aging formula in skin.

Unveiling the Nuances of Adult Female Acne: A Comprehensive Exploration of Epidemiology, Treatment Modalities, Dermocosmetics, and the Menopausal Influence.

Previously considered a skin disease exclusively affecting adolescents, characterized by inflammatory and non-inflammatory skin lesions, acne vulgaris is now increasingly observed in adult life, including post-menopause. Today, adult female acne (AFA) is a common chronic inflammatory disease of the pilosebaceous unit, with polymorphic lesions presenting as open or closed comedones, papules, pustules, and even nodules or cysts, often with the presence of sequelae. AFA may persist from adolescence or manifest de novo in adulthood. Its etiology is multifactorial, involving genetic, hormonal, dietary, and environmental factors, yet still incompletely understood. Increased sebum production, keratinocyte hyper-proliferation, inflammation, and reduced diversity of Cutibacterium acnes strains are the underlying disease mechanisms. During menopausal transition, a relative increase in androgen levels occurs, just as estrogens begin to decline, which can manifest itself as acne. Whereas most AFA exhibit few acne lesions with normo-androgenic serum levels, baseline investigations including androgen testing panel enable associated comorbidities to be eliminated, such as polycystic ovarian syndrome, congenital adrenal hyperplasia, or tumors. Another interesting feature is AFA's impact on quality of life, which is greater than in adolescents, being similar to other chronic diseases like asthma. The therapeutic approach to AFA depends on its severity and associated features. This review investigates the intricate facets of AFA, with a specific focus on incidence rates, treatment modalities, and the curious impact of menopause. Utilizing insights from contemporary literature and scientific discussions, this article seeks to advance our understanding of AFA, offering new perspectives to shape clinical practices and improve patient outcomes.