Atopic Dermatitis (AD) is a skin-associated disorder involving hyperactivation of inflammatory cascades. The attributing reasons to this include genetic predisposition, environmental factors and immunopathy. At the genetic level, there is an alteration in the filaggrin gene, which leads to impairment in the epidermal integrity. Hence, it makes the skin susceptible to irritants and allergens, causing skin barrier dysfunction, immune hypersensitivity and amplifying antigen penetration. However, at the molecular level the pathways altered in AD include T cell and cytokine pathway, Th2 pathways, IL pathway IL-4, IL-5, IL-13, Th1 pathway, IFN-γ cytokine pathway, Th17 pathway, IL-17 and IL-22 pathway, TGF-β pathway, JAK- STAT pathway, NFkB pathway, MAP2K2/ERK pathway, PI3K/Akt pathway, and Notch pathway. Overall, these events eventually lead to an increase in cytokine storm, keratinocytes proliferation, epidermal hyperplasia, fibrosis, oxidative stress and skin microbial imbalance. The present review highlights the molecular pathways associated with AD and discusses the crosstalk between inflammation, oxidative stress and genetic factors of AD. Moreover, understanding of these intricate pathways is necessary to develop a futuristic intervention to combat AD.
Keywords: Atopic condition; Atopic dermatitis; Barrier dysfunction; Filaggrin gene; Fuels inflammation; Genetic factors; Genetic risk factors; Inflammation; Microbiome; Neuropeptide; Oxidative stress; Pathogenesis; Signaling pathways; Toll-like receptors.
© 2025. The Author(s), under exclusive licence to Springer Nature Switzerland AG.