The pathophysiology of vascular calcification: are osteoclast-like cells the missing link?
Diabetes Metab
; 34 Suppl 1: S16-20, 2008 Feb.
Article
in En
| MEDLINE
| ID: mdl-18358422
ABSTRACT
There is increasing evidence to suggest that the initiation of vascular calcification is an active process involving vascular smooth muscle cell (VSMC) apoptosis and trans-differentiation into calcifying cells. This active process results in the deposition of an osteogenic extracellular matrix and may be exacerbated by a reduction in the levels of one or more native calcification inhibitors (such as fetuin A and pyrophosphate). Here, we present data which strongly suggest that the regression of vascular calcification might also be an active cellular process involving osteoclast-like cells. However, the presence of osteoclast like cells in the vascular wall is rather limited. To explain this rarity of osteoclast-like cells, we recently observed that the same factors, which promote the trans-differentiation of VSMCs into osteoblast-like cells are also capable of inhibiting the in vitro differentiation of monocytes/macrophages into osteoclast-like cells. An imbalance between osteoblast-like and osteoclast-like cell activities would therefore favour the occurrence of a pathological calcification process in vessel walls. Our new data are strongly evocative of a vascular remodelling process similar to that observed in bone tissue. To confirm this hypothesis, strategies for activating osteoclasts in the vascular wall (with a view to preventing or reversing vascular calcifications) are required.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Osteoclasts
/
Calcinosis
/
Cardiovascular Diseases
/
Muscle, Smooth, Vascular
Limits:
Humans
Language:
En
Journal:
Diabetes Metab
Journal subject:
ENDOCRINOLOGIA
/
METABOLISMO
Year:
2008
Type:
Article
Affiliation country:
France