Polycystins in disease mechanobiology.
cancer
craniosynostosis
endothelial dysfunction
mechanotransduction
osteoblast differentiation
polycystins
psoriasis
Journal
Journal of cellular biochemistry
ISSN: 1097-4644
Titre abrégé: J Cell Biochem
Pays: United States
ID NLM: 8205768
Informations de publication
Date de publication:
May 2019
May 2019
Historique:
revised:
29
10
2018
received:
15
10
2018
pubmed:
22
11
2018
medline:
22
11
2018
entrez:
22
11
2018
Statut:
ppublish
Résumé
Distorted mechanotransduction represents the molecular hallmark of disease mechanobiology and is displayed with common features during the development of various pathophysiologies. Polycystins constitute a family of mechanosensitive proteins that facilitate pathogenic signal transduction mechanisms. The main representatives of the family are polycystin-1 (PC1) and polycystin-2 (PC2), which function as a mechano-induced membrane receptor and a calcium-permeable ion channel, respectively. PC1 and PC2 mediate extracellular mechanical stimulation, induce intracellular molecular signaling and evoke corresponding gene transcription. Recent reports reveal that polycystin-mediated signaling does not occur in polycystic kidney disease only, where it is most prominently studied. It is also present during the development of clinical entities such as endothelial dysfunction and atheromatosis, deregulation of osteoblast differentiation, cancer development, and psoriasis. In this study, we highlight emerging data that support the overall contribution of polycystins to disease mechanobiology and suggest further exploration of this protein family in diseases generated from force-bearing tissue structures.
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
6894-6898Informations de copyright
© 2018 Wiley Periodicals, Inc.