Cell Death in Skin Function & Inflammation | Mechanisms, Pathways & Clinical Impact

 

1. Introduction

Cell death is a fundamental biological process essential for skin development, renewal, and immune defense. In healthy skin, tightly regulated cell death maintains epidermal balance, while dysregulation can trigger chronic inflammation and disease. Understanding these mechanisms is central to modern dermatological research.

2. Apoptosis and Skin Homeostasis

Apoptosis supports normal epidermal turnover by removing damaged or aged keratinocytes without provoking inflammation. This controlled form of cell death preserves skin barrier integrity and prevents immune overactivation, making it critical for long-term skin health.

3. Necroptosis and Inflammatory Signaling

Necroptosis is a programmed yet inflammatory form of cell death that releases danger signals into the skin microenvironment. Its activation is increasingly linked to psoriasis, dermatitis, and impaired wound repair, highlighting its role in inflammatory skin disorders.

4. Pyroptosis in Cutaneous Immunity

Pyroptosis occurs primarily in immune and epithelial cells and is driven by inflammasome activation. In skin tissue, this pathway amplifies inflammatory cytokine release, contributing to host defense while also promoting pathological inflammation when dysregulated.

5. Ferroptosis and Oxidative Stress in Skin

Ferroptosis is an iron-dependent form of cell death associated with lipid peroxidation and oxidative damage. Emerging research connects ferroptosis to skin aging, UV damage, and inflammatory responses, opening new avenues for antioxidant-based interventions.

6. Therapeutic and Future Research Directions

Targeting specific cell death pathways offers promising strategies for treating inflammatory skin diseases and improving wound healing. Future research aims to develop precision therapies that modulate cell death while preserving essential skin functions and immune balance.


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#MolecularDermatology
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