Within solar ultraviolet (UV) light, the longest UVA1 wavelengths, with significant and relatively constant levels all year round and large penetration properties, produce effects in all cutaneous layers. Their effects, mediated by numerous endogenous chromophores, primarily involve the generation of reactive oxygen species (ROS). The resulting oxidative stress is the major mode of action of UVA1, responsible for lipid peroxidation, protein carbonylation, DNA lesions and subsequent intracellular signaling cascades. These molecular changes lead to mutations, apoptosis, dermis remodeling, inflammatory reactions and abnormal immune responses. The altered biological functions contribute to clinical consequences such as hyperpigmentation, inflammation, photoimmunosuppression, sun allergies, photoaging and photocancers. Such harmful impacts have also been reported after the use of UVA1 phototherapy or tanning beds. Furthermore, other external aggressors, such as pollutants and visible light (Vis), were shown to induce independent, cumulative and synergistic effects with UVA1 rays. In this review, we synthetize the biological and clinical effects of UVA1 and the complementary effects of UVA1 with pollutants or Vis. The identified deleterious biological impact of UVA1 contributing to clinical consequences, combined with the predominance of UVA1 rays in solar UV radiation, constitute a solid rational for the need for a broad photoprotection, including UVA1 up to 400 nm.

/pdf/the-damaging-effects-of-long-uva-uva1-rays-a-major-challenge-1fv0lwb2.pdf

The Damaging Effects of Long UVA (UVA1) Rays: A Major Challenge to Preserve Skin Health and Integrity

Skin aging goes beyond a chronological process and also results from extrinsic factors referred to as the exposome. Hyaluronic acid (HA) is an important component of the extracellular matrix, with loss starting at 25 years old. While many studies of HA concern topical use, few literature reviews only address the use of topical HA in dermatology. This review describes the different characteristics of HA‐containing cosmeceuticals, with a focus on skin aging and the impact of exposome factors on HA synthesis and degradation. A review was performed using the terms HA, hyaluronan, topical, dermatology, cosmetic, aging treatment, exposome, and cosmeceuticals. Results are also presented from a recent randomized controlled trial (RCT), which investigated the additional benefit of using a HA epidermic filler (HA‐filler serum) combined with Botulinum toxin type A (BoNTA) to treat signs of skin aging. Subjects were randomized to two groups: HA‐filler serum starting 24 h after the BoNTA injection then twice daily for 24 weeks, or the control group, which received BoNTA. HA is a key ingredient used in cosmeceuticals for its hydration/antiaging properties (hygroscopic, rheological, and viscoelastic). Several clinical studies indicate that HA is both well tolerated and effective, adjuvant to both post‐surgical and facial rejuvenation procedures. In the RCT, one of few studies to combine BoNTA and HA with a 6‐month follow‐up, the HA‐filler serum lengthened the duration of BoNTA's effect in reducing wrinkles. Numerous studies support HA‐based cosmeceuticals as a noninvasive, effective solution for improving skin hydration and rejuvenation.

Benefits of topical hyaluronic acid for skin quality and signs of skin aging: From literature review to clinical evidence

Psychological stress is a crucial factor in the development of many skin diseases, and the stigma caused by skin disorders may further increase the psychological burden, forming a vicious cycle of psychological stress leading to skin diseases. Therefore, understanding the relationship between stress and skin diseases is necessary. The skin, as the vital interface with the external environment, possesses its own complex immune system, and the neuroendocrine system plays a central role in the stress response of the body. Stress-induced alterations in the immune system can also disrupt the delicate balance of immune cells and inflammatory mediators in the skin, leading to immune dysregulation and increased susceptibility to various skin diseases. Stress can also affect the skin barrier function, impair wound healing, and promote the release of pro-inflammatory cytokines, thereby exacerbating existing skin diseases such as psoriasis, atopic dermatitis, acne, and urticaria. In the present review, we explored the intricate relationship between stress and skin diseases from a neuroendocrine-immune interaction perspective. We explored the occurrence and development of skin diseases in the context of stress, the stress models for skin diseases, the impact of stress on skin function and diseases, and relevant epidemiological studies and clinical trials. Understanding the relationship between stress and skin diseases from a neuroendocrine-immune interaction perspective provides a comprehensive framework for targeted interventions and new insights into the diagnosis and treatment of skin diseases. 

Role of stress in skin diseases: A neuroendocrine-immune interaction view

A Transdermal Drug Delivery System Based on Nucleic Acid Nanomaterials for Skin Photodamage Treatment

Ferroptosis is a recognized novel form of programmed cell death pathway, featuring abnormalities in iron metabolism, SystemXc−/glutathione axis, and lipid peroxidation regulation. A variety of ferroptosis inducers can influence glutathione peroxidase directly or indirectly via diverse pathways, leading to decreased antioxidant capacity, accumulated cellular lipid peroxides, and finally inducing ferroptosis. To date, mounting studies confirm the association of ferroptosis with various cutaneous diseases, including skin homeostasis, neoplastic diseases, infectious diseases, genetic skin disease, inflammatory skin diseases, and autoimmune diseases. There are shared characteristics regarding ferroptosis and various cutaneous diseases in terms of pathophysiological mechanisms, such as oxidative stress associated with iron metabolism disorder and accumulated lipid peroxides. Therefore, we summarize the current knowledge regarding the mechanisms involved in the regulation of ferroptosis for further discussion of its role in the pathogenesis and prognosis of skin diseases. Gaining insight into the underlying mechanisms of ferroptosis and the associated dermatological disorders could illuminate the pathogenesis and treatments of different cutaneous diseases.

/pdf/ferroptosis-mechanism-and-connections-with-cutaneous-4tc0nbwu.pdf

Ferroptosis: Mechanism and connections with cutaneous diseases

Exposome factors that lead to stressed skin can be defined as any disturbance to homeostasis from environmental (meteorological factors, solar radiation, pollution or tobacco smoke) and/or internal exposure (unhealthy diet, hormonal variations, lack of sleep, psychosocial stress). The clinical and biological impact of chronic exposome effects on skin functions has been extensively reviewed, whereas there is a paucity of information on the impact of short-term acute exposure. Acute stress, which would typically last minutes to hours (and generally no more than a week), provokes a transient but robust neuroendocrine-immune and tissue remodeling response in the skin and can alter the skin barrier. Firstly, we provide an overview of the biological effects of various acute stressors on six key skin functions, namely the skin physical barrier, pigmentation, defenses (antioxidant, immune cell-mediated, microbial, and microbiome maintenance), structure (extracellular matrix and appendages), neuroendocrine, and thermoregulation functions. Secondly, we describe the biological and clinical effects on adult skin from individual exposome factors that elicit an acute stress response and their consequences in skin health maintenance. Clinical manifestations of acutely stressed skin may include dry skin that might accentuate fine lines, oily skin, sensitive skin, pruritus, erythema, pale skin, sweating, edema, as well as flares of inflammatory skin conditions such as acne, rosacea, atopic dermatitis, pigmentation disorders, and skin superinfection such as viral reactivation. Acute stresses can also induce scalp sensitivity, telogen effluvium, and worsen alopecia.

https://www.onlinelibrary.wiley.com/doi/pdf/10.1111/jdv.17432

Adult skin acute stress responses to short-term environmental and internal aggression from exposome factors

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Adult skin acute stress responses to short-term environmental and internal aggression from exposome factors