2018
DOI: 10.1080/08820139.2017.1423499
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Study of the osteoprotegerin/receptor activator of nuclear factor-kB ligand system association with inflammation and atherosclerosis in systemic sclerosis

Abstract: In cardiovascular risks, OPG serum level might increase as a preventive compensatory mechanism to neutralize the RANKL level increment. The determination of the OPG-RANKL system is a diagnostic indicator for the intensity of vascular calcification and atherosclerosis in SSc patients.

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Cited by 18 publications
(10 citation statements)
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“…18,33 Along with the ongoing process of atherosclerosis and in the late stages of lesion progress, OPG may cause some kind of injury to the vessels where it is incapable to reverse the process of vascular calcification. 18,34 It should be mentioned that OPG not only modulates RANKL but also acts in some RANKL-independent manners such as chemotaxis of monocytes. 35 In our study, there were no significant differences in serum levels as well as gene expression of OPG, RANK, and RANKL among different severity groups of UA according to TIMI and GRACE scores.…”
Section: Discussionmentioning
confidence: 99%
“…18,33 Along with the ongoing process of atherosclerosis and in the late stages of lesion progress, OPG may cause some kind of injury to the vessels where it is incapable to reverse the process of vascular calcification. 18,34 It should be mentioned that OPG not only modulates RANKL but also acts in some RANKL-independent manners such as chemotaxis of monocytes. 35 In our study, there were no significant differences in serum levels as well as gene expression of OPG, RANK, and RANKL among different severity groups of UA according to TIMI and GRACE scores.…”
Section: Discussionmentioning
confidence: 99%
“…Одним из возможных механизмов формирования АС, учитывая результаты настоящей работы, является нарушение чувствительности OPG к RANKL, второй возможной причиной является повышение концентрации sRANKL у больных с АС. Gamal RM, et al анализируя активность системы OPG/RANKL сделал вывод, что повышение OPG является компенсаторным механизмом, направленным на нейтрализацию sRANKL, а соотношение OPG/ RANKL может рассматриваться как диагностический индикатор тяжести сосудистой кальцификации и атеросклероза [12]. Подобной гипотезой можно объяснить и данные, полученные в нашем исследовании.…”
Section: Discussionunclassified
“…[8] RANKL is mainly secreted by osteoblast and activated T cells and binds to receptor activator of nuclear factor-kB (TNF Receptor Superfamily 11A, TNFRSF11A, RANK) to induce the maturation and activation of osteoclast precursors and motivate bone resorption. [9] Decoy receptor belonging to TNF receptor superfamily called osteoprotegerin (TNFRSF11B, OPG) inhibits the binding of RANKL to RANK then suppressing the osteoclastogenesis. [10] Imbalance of the RANKL/RANK/OPG concentration ratio is involved in bone remodeling and consequently loss of bone density in a large number of immune system diseases including osteoporosis [11] or RA.…”
Section: Introductionmentioning
confidence: 99%
“…Among cytokine families, receptor activator of nuclear factor‐κB ligand (RANKL), also known as tumor necrosis factor‐related activation‐induced cytokine (TRANCE), is a homotrimeric type II membrane protein member of the TNF‐α superfamily (TNF Superfamily 11, TNFSF11) . RANKL is mainly secreted by osteoblast and activated T cells and binds to receptor activator of nuclear factor‐κB (TNF Receptor Superfamily 11A, TNFRSF11A, RANK) to induce the maturation and activation of osteoclast precursors and motivate bone resorption . Decoy receptor belonging to TNF receptor superfamily called osteoprotegerin (TNFRSF11B, OPG) inhibits the binding of RANKL to RANK then suppressing the osteoclastogenesis .…”
Section: Introductionmentioning
confidence: 99%