Abstract:
The pathophysiology of atopic dermatitis (AD) is complex and multifactorial, primarily involving barrier dysfunction. Tight junctions (TJs) are intercellular junctions that are important for establishing the epithelial barrier and maintaining its polarity. Tight junctions have an essential role in the development and function of the stratum corneum, indicating that diseases with TJ dysfunction will cause a disruption on the stratum corneum homeostasis. Atopic dermatitis is a skin disorder that affects 20% of the human population. The complex interactions between damaged skin barrier, skin inflammation, and itching contribute to the development, progression, and duration of AD. Elevated epicutaneous sensitization and skin sensitivity to exogenous stimuli are both caused by skin barrier dysfunction. Desmosomes and TJs hold a complex matrix of structural proteins and lipids that make up the skin barrier together. These aspects form the foundation of barrier disruption in AD. The discovery of the TJ protein Claudin-1 plays a key role in human epidermal tissue and keratinocyte proliferation. Barrier disruption in patients with AD is not only confined to the stratum corneum but also to the TJs, and regulation of these barriers may provide opportunities for new therapies in people with AD or other atopic diseases.
Page(s):
648-654
DOI:
DOI not available
Published:
Journal: Journal of Pakistan Association of Dermatologists, Volume: 33, Issue: 2, Year: 2023
Keywords:
eolgtAtopic dermatitis
,
Human and health
,
Claudin1
,
Tight Junction