Galectin 3 is a unique ~31 kDa protein that recognizes the N-acetyl-lactosamine structure of several glycoconjugates. It mainly occurs in epithelial and myeloid cells, but is also found in a variety of human cell types. In view of the crucial role played by galectin 3 in the regulation of cellular processes of essential importance and in the pathogenetic mechanisms of diverse disorders, it is not surprising that, particularly in the last three decades, the attention of the scientific community has been increasingly drawn to this extraordinary and multifunctional galectin. In this paper the authors summarize current knowledge on the expression of galectin 3 in normal and diseased human skin, its implications in the pathogenesis, diagnosis and prognosis of cutaneous disorders, and the perspectives of a novel approach to the treatment of the latter using galectin 3 or its inhibitors/antagonists.
Atopic dermatitis (AD), psoriasis and senile xerosis comprise common chronic and relapsing inflammatory skin disorders with clinical symptoms such as lichenification, pruritus and inflammatory lesions that affect the quality of life of patients. In this study, we aimed to evaluate the efficacy of a novel "emollient plus" formulation (Lipikar baume AP+M), containing non-living lysates of non-pathogenic Vitreoscilla Filiformis bacteria from LaRoche-Posay Thermal Spring water, in improving quality of life, alleviating skin pain, and managing symptoms of mild-to-severe AD or skin disorders associated with dryness or severe xerosis in adults. The study included 1,399 adult patients, who participated in a two-month observational study over two visits, conducted at dermatologists' practices. Visits included clinical assessment of skin disease before and after administration of the product as well as completion of the 10-question Dermatology Life Quality Index. Questionnaires were used to evaluate efficacy, safety, satisfaction and tolerance of the product both by the dermatologists and patients, as well as assess quality of life of patients. Statistically significant improvement (p<0.001) by at least one grade was observed by more than 90% based on patients' evaluation of efficacy regarding intensity of the skin disease, skin dryness, surface affected by inflammatory lesions, pruritus, quality of sleep, daily discomfort, dryness and desquamation. Quality of life after two months improved by 82.6%. This study demonstrated significant reduction in symptoms of mild-to-severe skin dryness after application of the "emollient plus" formulation over two months, either alone or as adjunctive therapy.
Fibrotic diseases of the skin and lung, such as systemic sclerosis, hypertrophic scars, keloids, and pulmonary fibrosis, share core molecular mechanisms despite their distinct anatomical settings. Central to their pathogenesis are persistent fibroblast activation, immune dysregulation, ECM remodeling, and failure of resolution pathways, all modulated by an ever-changing environment and epigenetic regulation. Increasing evidence reveals that chronic injury from air pollution, ultraviolet radiation, climate stressors, and occupational hazards accelerates fibroinflammatory remodeling across these barrier organs. Moreover, shared signaling networks, including TGF-β, IL-4/IL-13, Wnt/β-catenin, and epigenetic regulators like miR-21 and miR-29, suggest convergent fibrotic programs may be subject to cross-organ therapeutic targeting. This review integrates recent insights into the exposome’s role in driving fibrosis, highlights novel RNA- and epigenetic-based interventions, and evaluates the repurposing of antifibrotic agents approved for pulmonary disease within dermatologic contexts. We emphasize the emerging concept of fibrosis-aware precision medicine and propose a unifying framework to guide integrated therapeutic strategies. In the face of global climate change and rising environmental insults, a cross-organ perspective on fibrosis offers a timely and translationally relevant approach to addressing this growing burden on human health.