The insulin‐like growth factor‐1 (IGF‐1) signaling pathway is known as a potent aging modifier, disruption of which consistently associates with lifespan extension across diverse species. Despite this established association, the mechanisms by which IGF‐1 signaling modulates organ aging remain poorly understood. In this study, we assessed age‐related changes in IGF‐1 expression across multiple organs in mice and identified a more prominent increase in skin IGF‐1 levels with aging—a phenomenon also observed in human skin. To explore the consequences of elevated IGF‐1, we developed transgenic mice ectopically expressing human IGF‐1 in the epidermis, driven by the bovine keratin 5 promoter (IGF‐1 Tg). These mice exhibited premature aging of hair follicles, as evidenced by accelerated hair graying and loss. Single‐cell RNA sequencing analyses of dorsal skin highlighted an upsurge in cellular senescence markers and the senescence‐associated secretory phenotype (SASP) in hair follicle stem cells (HFSCs), alongside a decline in hair growth and HFSC exhaustion. Our findings indicate that excessive IGF‐1 triggers HFSC senescence, thereby disrupting hair follicle homeostasis. Remarkably, interventions in IGF‐1 signaling via downstream mechanisms—specifically blocking Ac‐p53 activation via SIRT1 overexpression or senolytic treatment for senescent cell clearance, or reducing IGF‐1 through dietary restriction—significantly reduced senescence markers, mitigated premature hair follicle aging phenotypes, and restored the stem cell pool. Our findings provide fundamental insights into the biological processes of hair aging and highlight the therapeutic promise of targeted interventions to rejuvenate aged HFSCs and promote hair follicle health.

Abstract Aging is an inevitable natural process, with gray hair being one of its most visible signs. Hair graying holds psychosocial importance and is an excellent model for studying human pigmentation and aging in an accessible mini-organ. This phenomenon results from decreased melanin production in hair follicles, influenced by genetic, environmental, and lifestyle factors. Gray hair often poses aesthetic concerns and can be accelerated by environmental stressors, lifestyle choices, and nutritional deficiencies. Given the variation in onset and prevalence of gray hair, this study explores the underlying biological factors—namely, genetics, oxidative stress, and hormonal changes—to inform better prevention and treatment strategies. Recent advancements in prevention and treatment, such as topical melanin stimulants, antioxidants, dietary supplements, and low-level laser therapy (LLLT), offer promising approaches to managing gray hair. Understanding gray hair comprehensively—encompassing biological, psychological, and social dimensions—provides valuable insights into the aging process and can enhance overall well-being while addressing the stigma associated with aging. Our comprehensive analysis reveals that while graying correlates with certain health conditions, its primary significance is physiological rather than pathological. This understanding is essential for healthcare providers and the public to approach graying with scientific objectivity rather than social prejudice.

Graying of the hair before the age of 20 in Caucasians and before the age of 30 in African Americans is known as Premature Graying Hair (PGH) or Canities. It might have a negative impact on someone's Quality of Life. According to unani system it may be because of weakness of Hazm, poor nutrition of the hair and predominance of Burudat (coldness) in the body. The precise etiopathogenesis is yet unclear. When a patient has PGH, they should be evaluated for metabolic disorders and syndromes. According to Unani System the cause of premature greying of hair is excess production of Balgham (Phlegm) is increased greying of hair. Hair Colors and Colorants can be a transitory treatment choice however aggravation and unfavorably susceptible impacts to certain people are accounted for, it likewise expands the financial burdan. Treatment choices for PGH is calcium pantothenate, PABA, or both in blend and treating the going with obsessive circumstances. Natural Drugs, Nutritional supplements, Unani herbs for both oral and local hair dyes continue to be the primary method of treating cosmetic issues. This review paper explores the detail etiopathogenesis and management of PGH.

Hair, like the skin and the human body as a whole, is subject to aging processes, which can be roughly divided into 2 aspects: aging of the hair shaft and aging of the hair follicle. There are currently no drugs for the targeted treatment of graying hair with proven effectiveness, and their development is the subject of scientific research. As for the treatment of age-related hair changes, it includes specific pharmacological therapies for hair loss, such as topical application of minoxidil and inhibition of 5-alpha reductase, as well as correction of age-related general health problems affecting the condition of the hair, such as: diseases of the gastrointestinal tract with impaired absorption of nutrients necessary for hair fiber disorders, endocrine diseases, psychological disorders related to substance abuse, and polymorbidity. In addition to using external remedies, to prevent alopecia, strengthen the hair follicle and hair structure, it is of great importance to supply the body with nutrients that ensure the health of the skin and its appendages. There is every reason to consider modern Russian developments Osteomed and Osteo-Vit D3 as rich sources of such substances, which is the subject of our article.

During embryogenesis, the transcription factor, Sox10, drives the survival and differentiation of the melanocyte lineage. However, the role that Sox10 plays in postnatal melanocytes is not established. We show in vivo that melanocyte stem cells (McSCs) and more differentiated melanocytes express SOX10 but that McSCs remain undifferentiated. Sox10 knockout (Sox10fl; Tg(Tyr::CreER)) results in loss of both McSCs and differentiated melanocytes, while overexpression of Sox10 (Tg(DctSox10)) causes premature differentiation and loss of McSCs, leading to hair graying. This suggests that levels of SOX

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