2011
DOI: 10.1016/j.mehy.2011.08.015
|View full text |Cite
|
Sign up to set email alerts
|

Correlation of endothelin-1 mRNA expression and bone structure in advanced osteoarthritis

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1

Citation Types

0
2
0

Year Published

2013
2013
2024
2024

Publication Types

Select...
4

Relationship

1
3

Authors

Journals

citations
Cited by 4 publications
(3 citation statements)
references
References 18 publications
0
2
0
Order By: Relevance
“…There is certainly a lack of prospective evidence that links plaque characteristics to the rate of carotid restenosis. In order to overcome this, it is necessary to implement methodology similar to that found in some studies [18] using endarterectomised tissue samples. We speculate that the composition of an atherosclerotic plaque is directly responsible for the lesion's capacity to develop carotid restenosis.…”
Section: Resultsmentioning
confidence: 99%
“…There is certainly a lack of prospective evidence that links plaque characteristics to the rate of carotid restenosis. In order to overcome this, it is necessary to implement methodology similar to that found in some studies [18] using endarterectomised tissue samples. We speculate that the composition of an atherosclerotic plaque is directly responsible for the lesion's capacity to develop carotid restenosis.…”
Section: Resultsmentioning
confidence: 99%
“…One role and mechanism of hypertension in MetS is considered to be impaired bone metabolism due to interrupted blood flow in the subchondral bone, while another mechanism involves apoptosis of osteoblasts. 62,63 Recently, we showed that the renin–angiotensin system (RAS) component is expressed in mouse growth plates. 64 We also showed that the local RAS was involved in differentiation of chondrocytes in the ataxia–telangiectasia group D complementing cell line.…”
Section: Common Molecules Between Mets In Oa and Lox-1/ox-ldlmentioning
confidence: 99%
“…Bellisai et al [22] reported that ET-1 increases TNF-α synthesis in macrophages and monocytes, while Nakano et al [23] suggested that proinflammatory cytokines increase ET-1 expression. The induction of nitric oxide synthase by ET-1 leads to excessive nitric oxide production, activation of MMP-1 and MMP-13 synthesis, reduction of the interstitial fluid flow through a vasoconstrictive effect, and acceleration of cartilage destruction by the induction of osteocyte hypoxia leading to degeneration are among the hypotheses that aimed to explain the process [24]. It can be suggested that ET-1, a significant degeneration factor, could also be associated with lumbar pathologies.…”
Section: Introductionmentioning
confidence: 99%