The aging process is a complex succession of biological phenomena that, among others, cause epidermal thinning with a slowdown of its turnover. Concurrently, the dermis loses collagen and elastin, leading to the appearance of fine lines and wrinkles on the faces of both women and men who desire to maintain a youthful appearance and achieve a longer life. Consequently, there is a widespread pursuit of rejuvenation through the use of cosmeceuticals and nutraceuticals, aligning with the concept of “Beauty from Within”. This approach involves the contemporary use of the same active ingredients, applied topically via cosmetics and ingested orally through dietary supplements. This paper, by examining the structure and functions of the skin and mucous membranes and their associated aging phenomena, emphasizes the necessity of developing products that are effective and safe. Such products must possess the capacity to cross the barriers of these biological structures without provoking any side effects. To this end, novel tissue-carriers, fabricated from biodegradable polymers, are proposed as an integrated solution, creating advanced cosme-nutraceuticals that are not only highly effective and skin-friendly but also address the critical environmental challenge of plastic waste.
Chronic skin disease is highly prevalent in China and is frequently accompanied by psychological and metabolic comorbidities, yet primary healthcare systems remain insufficiently equipped to provide continuous and integrated management. This review examines how digital health can strengthen primary care dermatology and support general practitioners (GPs) in the prevention, early identification, treatment, follow-up, and comorbidity management of chronic skin disease. Drawing on literature from PubMed and Ovid MEDLINE, as well as relevant guidelines and policy documents, the review synthesizes current evidence on primary care dermatology, digital health technologies, and integrated care models. Recent advances indicate that artificial intelligence (AI)-assisted diagnosis, teledermatology, and digital follow-up tools can enhance diagnostic capacity, facilitate specialist-primary care collaboration, and improve continuous patient management and self-management support. These technologies may help primary care move beyond fragmented, single-visit care toward a more integrated, lifecycle-based model. However, important barriers remain, including limited dermatology training among GPs, insufficient infrastructure, fragmented referral pathways, and variability in digital literacy and resource availability. Overall, digital health provides an important opportunity to strengthen primary care-based dermatology services and integrated chronic disease management. Future efforts should focus on workforce capacity building, system integration, and patient empowerment to support more accessible, coordinated, and sustainable care for people with chronic skin disease.
Diabetic cutaneous wounds, particularly diabetic foot ulcers, are common and refractory chronic complications of diabetes. Their impaired healing is closely associated with persistent inflammation, oxidative stress, insufficient angiogenesis, dysregulated extracellular matrix (ECM) remodeling, and defective re-epithelialization. Re-epithelialization requires keratinocytes to undergo coordinated, stage-dependent transitions among activation, migration, proliferation, redifferentiation, and barrier reconstruction. Compared with the classical concept of epithelial–mesenchymal transition, epithelial–mesenchymal plasticity (EMP) more accurately reflects the transient, reversible, and intermediate phenotypic states adopted by keratinocytes during cutaneous wound repair. Exosomes/small extracellular vesicles (sEVs) may support this process by exerting functional effects on keratinocyte repair programs and indirectly remodeling inflammatory, vascular, oxidative, and ECM microenvironments. However, most available studies assess wound closure, histological re-epithelialization, angiogenesis, inflammation, or collagen deposition, and direct evidence linking exosome/sEV treatment to coordinated EMP-associated state transitions, epithelial redifferentiation, and barrier recovery in diabetic wound keratinocytes remains limited. This review therefore reinterprets current exosome/sEV evidence through a keratinocyte-centered framework of “EMP imbalance–exosome-mediated intercellular communication–wound microenvironment remodeling.” We distinguish direct EMP evidence from functional keratinocyte effects, indirect microenvironmental support, and mechanistic inference, and discuss engineered vesicles, local delivery systems, evidence maturity, and translational risks. This framework clarifies both the therapeutic promise and the current evidentiary boundaries of exosome/sEV-based strategies for diabetic wound re-epithelialization.
Background: Psoriatic arthritis (PsA) is a chronic progressive inflammatory arthritis associated with psoriasis, primarily affecting the spine and/or peripheral joints. Secukinumab is a fully human monoclonal antibody that inhibits interleukin-17A (IL-17A). In this study, we utilized musculoskeletal ultrasound (MSUS) to evaluate the therapeutic effects of secukinumab in treating moderate-to-severe plaque psoriasis patients with associated enthesitis.
Materials and methods: This single-center, retrospective study included 76 patients aged ≥ 18 years with moderate-to-severe plaque psoriasis and ultrasound-confirmed subclinical enthesitis, who were treated with secukinumab (300 mg) for 6 weeks.
Results: Secukinumab treatment resulted in significant improvements in skin lesions in patients with moderate-to-severe plaque psoriasis accompanied by subclinical enthesitis. Clinical assessments including Dermatology Life Quality Index (DLQI), body surface area (BSA), Psoriasis Area and Severity Index (PASI), and Investigator’s Global Assessment (IGA) showed a marked improvement. After 6 weeks of secukinumab treatment, MSUS assessments revealed significant decreases in the thickness of bilateral entheseal attachment points at the quadriceps tendon, inferior patellar margin, Achilles tendon, and plantar fascia at the calcaneus, with the most pronounced improvement observed in the right Achilles tendon attachment point (P = 2.71 × 10–9).
Discussion: Secukinumab rapidly improved cutaneous disease activity and reduced ultrasound-measured entheseal thickness in patients with moderate-to-severe plaque psoriasis and subclinical enthesitis. These findings suggest that IL-17A inhibition may help modulate early entheseal inflammation and support the use of MSUS for identifying and monitoring patients at risk of developing PsA.
Conclusions: Secukinumab significantly improves skin lesions and reduces entheseal thickness in patients with moderate-to-severe plaque psoriasis and subclinical enthesitis. These findings suggest a potential role for secukinumab in modifying early inflammatory processes and possibly delaying the progression to overt PsA, particularly in non-obese patients.
Background: Circadian rhythm disruption is increasingly recognized as a driver of systemic inflammation, yet the combined impact of lifestyle-related circadian imbalance and genetic predisposition on psoriasis risk remains poorly understood.
Objective: This study aimed to investigate the prospective association between a composite circadian imbalance index (CII) and incident psoriasis, and to evaluate its interaction with genetic risk.
Methods: The present prospective cohort included 260,118 participants from the UK Biobank. The primary study outcome was the incidence of psoriasis. Cox proportional hazards models were used to examine the association between CII and the risk of psoriasis. Sensitivity analyses, interaction analyses, and mediation analysis were performed.
Results: During a mean follow-up of 16.49 years, 2,519 incident psoriasis cases were identified. Higher CII was significantly associated with increased psoriasis risk. A significant additive interaction was observed between high CII and high polygenic risk score (PRS). Mediation analyses identified several blood biomarkers as partial mediators of this association.
Conclusions: Circadian imbalance represents a robust independent risk factor for psoriasis, especially among those with high genetic susceptibility. Given that this association is partially mediated by inflammatory and metabolic pathways, our findings suggest that optimizing circadian-related behaviors may serve as a critical preventive strategy.