Mechanotransduction in Skin Inflammation

Abstract

In the process of mechanotransduction, the cells in the body perceive and interpret mechanical stimuli to maintain tissue homeostasis and respond to the environmental changes. Increasing evidence points towards dysregulated mechanotransduction as a pathologically relevant factor in human diseases, including inflammatory conditions. Skin is the organ that constantly undergoes considerable mechanical stresses, and the ability of mechanical factors to provoke inflammatory processes in the skin has long been known, with the Koebner phenomenon being an example. However, the molecular mechanisms and key factors linking mechanotransduction and cutaneous inflammation remain understudied. In this review, we outline the key players in the tissue’s mechanical homeostasis, the available data, and the gaps in our current understanding of their aberrant regulation in chronic cutaneous inflammation. We mainly focus on psoriasis as one of the most studied skin inflammatory diseases; we also discuss mechanotransduction in the context of skin fibrosis as a result of chronic inflammation. Even though the role of mechanotransduction in inflammation of the simple epithelia of internal organs is being actively studied, we conclude that the mechanoregulation in the stratified epidermis of the skin requires more attention in future translational research.

Poly‐L‐Lactic acid increases collagen gene expression and synthesis in cultured dermal fibroblast (Hs68) through the TGF‐β/Smad pathway

“…In our study, elastin levels were also found to increase gradually with increasing PLLA concentration. Previous studies have confirmed that elastin, a type of dermal ECM cross‐linked fiber, together with collagen, forms the thicker connective tissue of the dermis, proving the mechanical framework and elasticity needed for the skin 24,25 . Therefore, cosmetic skin materials should mainly be biomaterials based on collagen and elastin.…”

Snail Slime Extracted by a Cruelty Free Method Preserves Viability and Controls Inflammation Occurrence: A Focus on Fibroblasts

“…They modify mechanosensitive pathways which, in turn, impacts skin homeostasis. At the same time, in some patients intrinsic factors including autoimmune responses, mutations, and others, can be responsible for inflammatory skin disorders [ 13 ]. For instance, the two most diffuse inflammatory skin conditions mediated by autoimmune response are psoriasis and atopic dermatitis, both involving T-cells [ 14 ].…”

Inflammation modulates intercellular adhesion and mechanotransduction in human epidermis via ROCK2

“… 1 , 2 , 3 , 4 , 5 , 6 In contrast, the compromised epidermal barrier in inflamed skin, such as in psoriasis and atopic dermatitis, is explained mainly by the improper keratinocyte differentiation, sphingolipid synthesis, and, as a result, the malformation of the cornified layer in the multi-layered epidermis. 7 , 8 , 9 , 10 , 11 , 12 , 13 …”

“…To the present date, the regulation and interconnection of cell-cell adhesion, cell contractility, and the downstream mechanosignaling in inflamed epidermis remain unclear. 13 At the same time, innovative topical therapies for chronic inflammatory skin conditions such as psoriasis are much needed. 74 In this study, we have modeled psoriatic inflammation using a specific cytokine stimulation 75 of non-differentiated human keratinocytes and reconstructed human epidermis (RHE), which closely reproduces epidermal differentiation and stratification processes.…”