Italian
Albanian
Arabic
Armenian
Azerbaijani
Belarusian
Bengali
Bosnian
Catalan
Czech
Danish
Deutsch
Dutch
English
Estonian
Finnish
Français
Greek
Haitian Creole
Hebrew
Hindi
Hungarian
Icelandic
Indonesian
Irish
Italian
Japanese
Korean
Latvian
Lithuanian
Macedonian
Mongolian
Norwegian
Persian
Polish
Portuguese
Romanian
Russian
Serbian
Slovak
Slovenian
Spanish
Swahili
Swedish
Turkish
Ukrainian
Vietnamese
Български
中文(简体)
中文(繁體)
Experimental Dermatology 2013-Mar

Impaired Notch-MKP-1 signalling in hidradenitis suppurativa: an approach to pathogenesis by evidence from translational biology.

Solo gli utenti registrati possono tradurre articoli
Entra registrati
Il collegamento viene salvato negli appunti
Bodo C Melnik
Gerd Plewig

Parole chiave

Astratto

Recent findings in familial hidradenitis suppurativa (HS) demonstrated loss-of-function mutations of components of the γ-secretase (GS) complex leading to decreased protease cleaving activity, which may compromise canonical Notch signalling. Appropriate Notch signalling is of pivotal importance for maintaining the inner and outer root sheath of the hair follicle and skin appendages. This viewpoint on the pathogenesis of HS is primarily supported by circumstantial evidence derived from translational biology. Impaired Notch signalling is proposed to be the major pathogenic mechanism of HS. Deficient Notch signalling switches the fate of outer root sheath cells, resulting in conversion of hair follicles to keratin-enriched epidermal cysts. Impaired Notch signalling may compromise apocrine gland homoeostasis as well. Damage-associated molecular pattern molecules released by either ruptured epidermal cysts exposing keratin fibres or altered structural components of less maintained apocrine glands may both stimulate TLR-mediated innate immunity. All aggravating factors of HS, that is, smoking, obesity, skin occlusion, androgens and progesterone, may further promote inflammation by release of proinflammatory cytokines derived from activated monocyte/macrophages. Inappropriate Notch signalling may not only initiate inflammation in HS but may lead to insufficient feedback inhibition of overstimulated innate immunity. Regular Notch signalling via induction of MAPK phosphatase-1 (MKP-1) terminates TLR-MAPK-signalling in macrophages and IL-23 secreting DCs, the key players for Th17 cell polarization. Thus, impaired Notch signalling links HS to other Th17-driven comorbidities. All major therapeutic interventions in HS appear to attenuate increased MAPK activation of innate immune cells due to impaired Notch-mediated feedback regulation of innate immunity.

Unisciti alla nostra
pagina facebook

Il database di erbe medicinali più completo supportato dalla scienza

  • Funziona in 55 lingue
  • Cure a base di erbe sostenute dalla scienza
  • Riconoscimento delle erbe per immagine
  • Mappa GPS interattiva - tagga le erbe sul luogo (disponibile a breve)
  • Leggi le pubblicazioni scientifiche relative alla tua ricerca
  • Cerca le erbe medicinali in base ai loro effetti
  • Organizza i tuoi interessi e tieniti aggiornato sulle notizie di ricerca, sperimentazioni cliniche e brevetti

Digita un sintomo o una malattia e leggi le erbe che potrebbero aiutare, digita un'erba e osserva le malattie ei sintomi contro cui è usata.
* Tutte le informazioni si basano su ricerche scientifiche pubblicate

Google Play badgeApp Store badge