Background: The The nuclear receptor PPAR- has several roles in controlling metabolic and cellular activities. Recent years have brought increased focus on the roles played by inflammation, lipid metabolism, and immune response regulation in the development of dermatological diseases. PPAR- has several functions in skin biology, and expanding our knowledge of these might help in the treatment of a variety of skin problems. This review aims to evaluate the role of PPAR- in skin diseases. We also discuss its significance in skin biology, from keratinocyte regulation to sebaceous gland function. The use of PPAR- agonists in the treatment of inflammatory skin disorders, viral infections, autoimmune diseases, and hair difficulties is something we want to raise awareness of. PPAR- is emerging as a complicated player in dermatology, and our findings demonstrate its profound impact on skin health and disease. This protein regulates inflammation, lipid metabolism, and the immune response, making it a promising therapeutic target. Psoriasis, atopic dermatitis, and scarring alopecia may all benefit from PPAR- agonists in the future as new therapy alternatives.
Keywords: PPAR-γ; Conditions affecting the skin; swelling; lipid metabolism; the immune response.
Introduction
Alopecia The hair follicle is preserved and hair loss is temporary in alopecia areata, an autoimmune condition. When hair loss is severe, it often follows a relapsing-remitting pattern that may be chronic (5).
Alopecia areata is a mysterious aetiology that has yet to be determined. Alopecia areata, it is generally believed, is a T-cell-mediated autoimmune illness that is more common in those with a certain genetic predisposition (8).
It has been hypothesised that endogenous or external triggers initiate and numerous substances cooperate to sustain a T-cell driven autoimmune process. Based on what we know about its origins, hair loss is caused by a complicated cycle of inflammation that feeds on itself. The cytokines secreted by the keratinocytes trigger the endothelial cells to become activated, which then attract the T cells and macrophages, which in turn secrete even more cytokines. (2).
A breakdown of this immunological privilege zone due to an unidentified autoantigen has been postulated to underlie alopecia areata. Once IFN- and IL-2 are present, CD8+, CD4+, and other inflammatory cells may be induced to enter the immunological privilege zone. All of these changes may cause hair follicle irritation, which can lead to hair loss (5).
Upregulation of pro-inflammatory cytokines must play a crucial role in the pathogenesis of AA, just as it does in other autoimmune disorders. Overexpression of ICAM-1 and MHC molecules on hair follicle keratinocytes and dermal papilla cells, as well as abnormal lesional expression of tumour necrosis factor-(, interferon-(, IL-2, and IL-1, are all features of the immune response in AA. Increased levels of IL-1, IL-6, IL-15, IL-17A, and IFN- were seen in the blood of individuals with AA. (3).
PPARs are a subfamily of ligand-activated nuclear receptors that control gene transcription in response to dietary fatty acids. Different genes code for and distribute the three PPAR isoforms: PPAR-, PPAR-/, and PPAR-. PPAR- functions as an anti-inflammatory agent, aids in the differentiation and storage of fat in adipose tissue, and controls glucose metabolism via insulin sensitization (5).
In addition to its role in regulating inflammation, PPAR- has been connected to the function of sebaceous glands. The sebaceous glands' role in producing sebum is essential to the normal life cycle of hair follicles. Inflammatory responses often occur in pilo-sebaceous units, which are created alongside hair follicles (7). Many aspects of the inflammatory response are suppressed by PPAR- because it modulates cytokine expression. T cells, monocytes/macrophages, vascular smooth muscle cells, and endothelial cells all use different receptors and adhesion molecules (1). TNF-(, IL-1, lL-6, RANTES, and MCP-I are all inflammatory cytokines that are inhibited by PPAR- agonists in macrophages (4).
Hair matrix keratinocytes, hair shaft cortex, hair cuticle, inner root sheath, outer root sheath, dermal papilla cells, sebocytes, and the connective tissue sheath all express PPAR- in human skin (5).
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