# PPARγ: a key orchestrator of epidermal barrier, immune responses, and lipid metabolism in atopic dermatitis pathogenesis and therapy

## TL;DR

This paper reviews how PPARγ could be a key target for treating atopic dermatitis by influencing skin barrier, immunity, and lipid balance.

## Contribution

The paper provides a comprehensive review of PPARγ's role in AD pathogenesis and its potential as a novel therapeutic target.

## Key findings

- PPARγ influences epidermal barrier function and lipid metabolism in atopic dermatitis.
- PPARγ modulates immune responses and cutaneous microbiome in AD.
- PPARγ shows promise as a therapeutic target for AD treatment.

## Abstract

Atopic dermatitis (AD) is an immune-mediated inflammatory dermatosis characterized by epidermal barrier dysfunction, immune dysregulation, and cutaneous microbial dysbiosis. Existing therapeutic modalities for AD are limited in efficacy and durability, highlighting an unmet clinical need for novel, safe, and effective treatment strategies. Peroxisome proliferator-activated receptor gamma (PPARγ), a pivotal nuclear receptor involved in metabolic and inflammatory regulation, has emerged as a promising therapeutic target for AD. Its pleiotropic mechanisms encompass the restoration of stratum corneum integrity, modulation of aberrant immunoinflammatory signaling, normalization of cutaneous lipid metabolism, and regulation of the cutaneous microbiome and neuroimmune circuitry. This review comprehensively synthesizes the mechanistic evidence linking PPARγ to AD pathogenesis and critically appraises its potential as a novel therapeutic.