Recent advances in the role of Yes‐associated protein in dermatosis

Abstract

Background: Dermatosis is a general term for diseases of the skin and skin appendages including scleroderma, psoriasis, bullous disease, atopic dermatitis, basal cell carcinoma, squamous cell carcinoma, and melanoma. These diseases affect millions of individuals globally and are a serious public health concern. However, the pathogenesis of skin diseases is not fully understood, and treatments are not optimal. Yes-associated protein (YAP) is a transcriptional coactivator that plays a role in the regulation of gene transcription and signal transduction. Aims:To study the role of Yes-associated protein in skin diseases. Materials and Methods:The present review summarizes recent advances in our understanding of the role of YAP in skin diseases, current treatments that target YAP, and potential avenues for novel therapies.Results: Abnormal YAP expression has been implicated in occurrence and development of dermatosis. YAP regulates the cell homeostasis, proliferation, differentiation, apoptosis, angiopoiesis, and epithelial-to-mesenchymal transition, among other processes. As well as, it serves as a potential target in many biological processes for treating dermatosis. Conclusions:The effects of YAP on the skin are complex and require multidimensional investigational approaches. YAP functions as an oncoprotein that can promote the occurrence and development of cancer, but there is currently limited information on the therapeutic potential of YAP inhibition for cancer treatment. Additional studies are also needed to clarify the role of YAP in the development and maturation of dermal fibroblasts; skin barrier function, homeostasis, aging, and melanin production; and dermatosis.

The Pressurized Skin: A Review on the Pathological Effect of Mechanical Pressure on the Skin from the Cellular Perspective

“…This finding highlights the role of fibroblasts in the mechanical process of pathological melanoma cell proliferation, beyond the known keratinocyte-melanocyte crosstalk, and suggests their contribution to cancer development. Additionally, if epidermal stem cells are deficient in the inhibitor of plexin-B, the inhibition of YAP would be compromised, resulting in the cells' inability to sense mechanical pressure, which further disinhibits YAP [72]. This disinhibition can lead to cellular proliferation, potentially contributing to the development of basal cell carcinoma (BCC) [72].…”

“…Additionally, if epidermal stem cells are deficient in the inhibitor of plexin-B, the inhibition of YAP would be compromised, resulting in the cells' inability to sense mechanical pressure, which further disinhibits YAP [72]. This disinhibition can lead to cellular proliferation, potentially contributing to the development of basal cell carcinoma (BCC) [72]. In an in vitro study utilizing spiny mice (Acomys cahirinus) applied to human fibroblasts, treatment with verteporfin, a nuclear YAP-TEAD inhibitor, led to persistent enhancement of myofibroblast differentiation mediated by TGF-β, resulting in tissue fibrosis rather than regeneration; conversely, forcibly increasing YAP activity might prevent and rescue this process [73].…”

TAZ acting as a potential pathogenic biomarker to promote the development of lichen planus

“…Current studies have shown that TAZ is involved in the occurrence and development of a variety of neoplastic diseases 4 . In addition, TAZ is also related to the maintenance of inflammatory diseases 5–8 . However, its role and molecular mechanisms in lichen planus remain to be elucidated.…”

“… 4 In addition, TAZ is also related to the maintenance of inflammatory diseases. 5 , 6 , 7 , 8 However, its role and molecular mechanisms in lichen planus remain to be elucidated. Herein, we preliminarily explained the expression of TAZ in lichen planus, and analyzed the correlation between TAZ expression and the clinical features of lichen planus patients to explore the possible mechanism of TAZ in the occurrence and development of lichen planus.…”

Hyaluronic acid-modified and verteporfin-loaded polylactic acid nanogels promote scarless wound healing by accelerating wound re-epithelialization and controlling scar formation

“…Recently, the mechanism of scar formation has been reported to be the persistent activation of Yes-associated protein (YAP) that up-regulates fibrosis and leads to excessive ECM deposition [ 7 , 8 ]. Thus, YAP inhibition could represent a therapeutic strategy to suppress fibrosis in the treatment of various fibrosis diseases [ 9 , 10 ]. Verteporfin (VP), a Food and Drug Administration (FDA) approved porphyrin compound, has confirmed to inhibit YAP expression, suppress fibrosis and yield scarless skin regeneration [ 11 , 12 ].…”