Host cutaneous inflammatory and oxidative stress pathways

Host cutaneous inflammatory and oxidative stress pathways represent a complex network of signaling cascades that maintain skin homeostasis in response to environmental and endogenous stressors. The inflammatory component is primarily regulated by transcription factors such as Nuclear factor kappa B (NF-κB) and Activator protein 1 (AP-1), which induce the expression of pro-inflammatory cytokines like TNF-α, IL-1β, and IL-6 [PMID: 21848415]. Simultaneously, oxidative stress pathways involve the production of reactive oxygen species (ROS) that can damage cellular components and activate the Mitogen-activated protein kinase (MAPK) pathways [StatPearls]. To counteract this, the Nuclear factor erythroid 2-related factor 2 (Nrf2) pathway serves as a master regulator of the antioxidant response, inducing enzymes like Heme oxygenase-1 (HO-1) and Superoxide dismutase [PMID: 24513307]. Dysregulation of these pathways is a central feature of chronic skin diseases, including atopic dermatitis, psoriasis, and various forms of dermatitis, as well as skin aging and carcinogenesis [PMID: 30235095]. Therapeutic targeting of these pathways involves a variety of agents, ranging from broad-spectrum anti-inflammatories like corticosteroids to specific biologics and small-molecule inhibitors of JAK/STAT signaling [PubMed]. Additionally, antioxidant therapies aim to neutralize ROS and bolster the skin's endogenous defense mechanisms to prevent tissue damage and promote healing [PubChem].

Other names

Skin inflammatory responseCutaneous oxidative stress signalingDermal redox and inflammatory pathways

Modulation of pro-inflammatory cytokine production, inhibition of NF-κB signaling, and activation of the Nrf2-mediated antioxidant response element (ARE) pathway.