Serum carboxy-terminal telopeptide of type I collagen levels are associated with carotid atherosclerosis in patients with cardiovascular risk factors

Kondo, Takeshi; Endo, Itsuro; Aihara, Ken‐ichi; Onishi, Yukiyo; Dong, Bingzi; Ohguro, Yukari; Kurahashi, Kiyoe; Yoshida, Sumiko; Fujinaka, Yuichi; Kuroda, Akio; Matsuhisa, Munehide; Fukumoto, Seiji; Matsumoto, Toshio; Abe, Masahiro

doi:10.1507/endocrj.ej15-0589

Cited by 6 publications

(4 citation statements)

References 27 publications

(29 reference statements)

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“…We have shown that elevated levels of the glycation end-product carboxymethyl-lysine (CML) predict hip fracture risk independent of BMD (36). cIMT is also positively related to serum levels of C-terminal telopeptide of type I collagen, a marker of increased bone resorption (37) and with reduced perfusion of the vertebral skeleton (38). …”

Section: Discussionmentioning

confidence: 99%

The associations of subclinical atherosclerotic cardiovascular disease with hip fracture risk and bone mineral density in elderly adults

et al. 2018

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Section: Discussionmentioning

confidence: 99%

The associations of subclinical atherosclerotic cardiovascular disease with hip fracture risk and bone mineral density in elderly adults

et al. 2018

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“…29) Collagen I and collagen VIII are believed to be pathogenic ECM components leading to atherosclerosis. 30,31) Collagen I itself could promote the proliferation and migration of VSMCs. 32) It was reported that in the atherosclerotic plaque, collagen VIII was produced by VSMCs abundantly.…”

Section: Discussionmentioning

confidence: 99%

Novel ASK1 Inhibitor AGI-1067 Attenuates AGE-Induced Fibrotic Response by Suppressing the MKKs/p38 MAPK Pathway in Human Coronary Arterial Smooth Muscle Cells

et al. 2018

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The phenotype shifting of vascular smooth muscle cells (VSMCs) was indicated to play a role during the initial stage of atherosclerotic plaque formation by facilitating extracellular matrix deposition. This study was aimed at investigating the involvement of the apoptosis signal-regulating kinase 1 (ASK1)/mitogen-activated protein kinase (MAPK) kinases (MKKs)/p38 MAPK pathway in the advanced glycation end product (AGE)induced fibrotic response of VSMCs. The effect of the novel ASK1 inhibitor AGI-1067 was also studied.Cultured human coronary smooth muscle cells (HCSMCs) were exposed to AGEs. AGI-1067 and siRNAs silencing mkk3, mkk6, and p38 mapk were used to treat the cells. The activation of MKK3, MKK6, and p38 MAPK was assessed by immunoblotting. Fibrotic response was assessed by the fluorescence immunohistochemistry staining of collagen I and collagen VIII. Activation of immunoprecipitation determined the association of ASK1 and its inhibitor thioredoxin. A kinase assay was used to determine ASK1 activity.AGE incubation significantly activated ASK1, MKK3, and MKK6, which led to activation of p38 MAPK, resulting in upregulated fibrotic response in HCSMCs. However, siRNAs knocking down mkk3, mkk6, and p38 mapk impaired this fibrotic response. AGI-1067 administration not only dramatically inhibited the activation of ASK1/MKKs/p38 MAPK but also suppressed the expression of the downstream proteins, including transforming growth factor-β1, connective tissue growth factor, collagen I, and collagen VIII in HCSMCs exposed to AGEs.The ASK1/MKKs/p38 MAPK pathway was activated by AGEs, leading to the fibrotic response in VSMCs. AGI-1067 reversed this process by maintaining the inactive state of ASK1.

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“…In 50 of 63 studies, arterial stiffness was assessed as pulse wave velocity (PWV) based on pulse transit time. In contrast to the common carotid-femoral PWV (used in 42 studies), which is considered the gold standard for arterial stiffness assessment (145), 6 (of 50) studies considered PWV over the brachial-ankle trajectory (4,43,61,67,68,158). Although the brachial-ankle and carotid-femoral trajectories are different, both measures appear to correlate reasonably well (24).…”

Section: Content Analysis Of Selected Papersmentioning

confidence: 99%

Constitutive interpretation of arterial stiffness in clinical studies: a methodological review

Reesink

Spronck

2019

American Journal of Physiology-Heart and Circulatory Physiology

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Clinical assessment of arterial stiffness relies on noninvasive measurements of regional pulse wave velocity or local distensibility. However, arterial stiffness measures do not discriminate underlying changes in arterial wall constituent properties (e.g., in collagen, elastin, or smooth muscle), which is highly relevant for development and monitoring of treatment. In arterial stiffness in recent clinical-epidemiological studies, we systematically review clinical-epidemiological studies (2012–) that interpreted arterial stiffness changes in terms of changes in arterial wall constituent properties (63 studies included of 514 studies found). Most studies that did so were association studies (52 of 63 studies) providing limited causal evidence. Intervention studies (11 of 63 studies) addressed changes in arterial stiffness through the modulation of extracellular matrix integrity (5 of 11 studies) or smooth muscle tone (6 of 11 studies). A handful of studies (3 of 63 studies) used mathematical modeling to discriminate between extracellular matrix components. Overall, there exists a notable gap in the mechanistic interpretation of stiffness findings. In constitutive model-based interpretation, we first introduce constitutive-based modeling and use it to illustrate the relationship between constituent properties and stiffness measurements (“forward” approach). We then review all literature on modeling approaches for the constitutive interpretation of clinical arterial stiffness data (“inverse” approach), which are aimed at estimation of constitutive properties from arterial stiffness measurements to benefit treatment development and monitoring. Importantly, any modeling approach requires a tradeoff between model complexity and measurable data. Therefore, the feasibility of changing in vivo the biaxial mechanics and/or vascular smooth muscle tone should be explored. The effectiveness of modeling approaches should be confirmed using uncertainty quantification and sensitivity analysis. Taken together, constitutive modeling can significantly improve clinical interpretation of arterial stiffness findings.

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Serum carboxy-terminal telopeptide of type I collagen levels are associated with carotid atherosclerosis in patients with cardiovascular risk factors

Cited by 6 publications

References 27 publications

The associations of subclinical atherosclerotic cardiovascular disease with hip fracture risk and bone mineral density in elderly adults

The associations of subclinical atherosclerotic cardiovascular disease with hip fracture risk and bone mineral density in elderly adults

Novel ASK1 Inhibitor AGI-1067 Attenuates AGE-Induced Fibrotic Response by Suppressing the MKKs/p38 MAPK Pathway in Human Coronary Arterial Smooth Muscle Cells

Constitutive interpretation of arterial stiffness in clinical studies: a methodological review

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