Sclerostin and Vascular Pathophysiology.
Wnt
aging
atherosclerosis
calcification
cardiovascular
chronic kidney disease
diabetes mellitus
sclerostin
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
06 Jul 2020
06 Jul 2020
Historique:
received:
23
05
2020
revised:
26
06
2020
accepted:
03
07
2020
entrez:
10
7
2020
pubmed:
10
7
2020
medline:
9
3
2021
Statut:
epublish
Résumé
There is cumulating evidence for a contribution of Wnt signaling pathways in multiple processes involved in atherosclerosis and vascular aging. Wnt signaling plays a role in endothelial dysfunction, in the proliferation and migration of vascular smooth muscle cells (VSMCs) and intimal thickening. Moreover, it interferes with inflammation processes, monocyte adhesion and migration, as well as with foam cell formation and vascular calcification progression. Sclerostin is a negative regulator of the canonical Wnt signaling pathway and, accordingly, the consequence of increased sclerostin availability can be disruption of the Wnt signalling cascade. Sclerostin is becoming a marker for clinical and subclinical vascular diseases and several lines of evidence illustrate its role in the pathophysiology of the vascular system. Sclerostin levels increase with aging and persist higher in some diseases (e.g., diabetes, chronic kidney disease) that are known to precipitate atherosclerosis and enhance cardiovascular risk. Current knowledge on the association between sclerostin and vascular diseases is summarized in this review.
Identifiants
pubmed: 32640551
pii: ijms21134779
doi: 10.3390/ijms21134779
pmc: PMC7370046
pii:
doi:
Substances chimiques
Adaptor Proteins, Signal Transducing
0
Biomarkers
0
SOST protein, human
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
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