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العنوان
Hypoxia inducible factor 1 expression in patients with hidradenitis suppurativa/
المؤلف
Moussa, Doaa Helmy Ahmed.
هيئة الاعداد
باحث / دعاء حلمي أحمد موسي
مشرف / أسامة احمد سرور
مشرف / أشرف محمود حمزة
مشرف / نجلاء فتحى عجمية
مشرف / سمر نبيل العشى
الموضوع
Dermatology. Venereology. Andrology.
تاريخ النشر
2022.
عدد الصفحات
99 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب
تاريخ الإجازة
19/6/2022
مكان الإجازة
جامعة الاسكندريه - كلية الطب - Dermatology, Venereology and Andrology
الفهرس
Only 14 pages are availabe for public view

from 121

from 121

Abstract

Hidradenitis suppurativa is a chronic inflammatory skin disease affecting apocrine gland bearing skin such as axillae, inguinal, anogenital and submammary regoins. It is characterized by follicular occlusion, inflammation and rupture of hair follicles with subsequent suppuration, sinus tracts and hypertrophic scarring. Histological findings of HS show psoriasiform epidermal hyperplasia with extended rete ridges but without parahyperkeratosis or alterations of the stratum granulosum.
Hypoxia inducible factor-1α (HIF-1α) is a transcriptional regulator that orchestrates the cellular response to low oxygen stress. As a transcription factor, it affects and regulates the expression of genes involved in maintaining homeostasis as oxygen concentrations change. HIF-1 also mediates cellular responses to hypoxia by regulating glucose uptake and anaerobic respiration in oxygen-depleted environments.
HIF-1 plays a role in inflammation as its overexpression results in increased localized inflammation. Clear evidence suggests the involvement of pro-inflammatory cytokines in immune dysregulation in HS, with elevated levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-17 and interferon (IFN)-γ observed in HS lesions.
The augmented HIF-1 DNA binding activity after IL-1β and TNF-α treatments can be attributed to the increased HIF-1α protein level in the nuclei.
The use of TNF-α inhibitors have been associated with improvements in immune dysregulation in HS and support the importance of local molecular drivers in the pathogenesis of HS.