2015
DOI: 10.1016/j.joca.2015.04.026
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Characterization of diabetic osteoarthritic cartilage and role of high glucose environment on chondrocyte activation: toward pathophysiological delineation of diabetes mellitus-related osteoarthritis

Abstract: OA cartilages from DM patients showed increased responsiveness to IL-1β-induced inflammation. Accordingly, high glucose enhanced IL-1β-induced inflammation in cultured chondrocytes via oxidative stress and the polyol pathway. High glucose and diabetes may thus participate in the increased inflammation in OA.

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Cited by 102 publications
(88 citation statements)
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References 46 publications
(30 reference statements)
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“…At the level of expression by chondrocytes mRNA of IL-6 and COX-2, and at the level of production IL-6, and PGE 2 , and NO can influence the level of glucose in culture media. The production of IL-6 by chondrocytes rapidly decreased under addition in culture media Cytochalasin B (the glucose transport inhibitor) [16]. Authors [17], demonstrated effect of glucose levels in culture media on human chondrocytes functional activity.…”
Section: Discussionmentioning
confidence: 99%
“…At the level of expression by chondrocytes mRNA of IL-6 and COX-2, and at the level of production IL-6, and PGE 2 , and NO can influence the level of glucose in culture media. The production of IL-6 by chondrocytes rapidly decreased under addition in culture media Cytochalasin B (the glucose transport inhibitor) [16]. Authors [17], demonstrated effect of glucose levels in culture media on human chondrocytes functional activity.…”
Section: Discussionmentioning
confidence: 99%
“…Некоторые исследователи склонны рассматривать МетОА только как следствие избыточной нагрузки на опорные суставы вследствие ожирения [19]. Однако многие недавние исследования продемонстрировали, что адипокины, продуцируемые жировой тканью, гипергликемия, инсулинорезистент-ность и дислипидемия могут нарушать метаболизм суставных тканей, впрочем, как и других органов [1,4,8,10,21]. В последние годы также установлены но-вые механизмы, связывающие ОА с метаболическими заболеваниями: прямая взаимосвязь инсулинорези-стентности и синовиального воспаления; роль окис-ленных липопротеидов низкой плотности (ЛПНП) в формировании очагов жирового повреждения кости и поддержания воспаления синовиальной оболочки; потенциальное вовлечение кишечной микрофлоры и наличие циркадных ритмов [14].…”
Section: ë³êàðþ ùî ïðàêòèêóº / To General Practitionerunclassified
“…T1DM patients showed a decrease in antioxidants defenses and an increase in biomarkers of oxidative damage (Kasznicki et al, 2012). In addition, proinflammatory biomarkers IL-6 and TNF-α are significant predictors of knee OA (Livshits et al, 2009;Kou & Wu, 2014) and OA cartilages from DM patients showed increased responsiveness to IL-1β-induced inflammation via oxidative stress and polyol pathway thus participate in the increased inflammation in OA (Laiguillon et al, 2015). On the other hand, chondroprotective agents such as the antioxidants have been found to promote cartilage repair by stimulating anabolic metabolism of chondrocytes and/or inhibiting catabolic processes found in OA (Altman et al, 1987;Bhattacharya et al, 2012).…”
Section: Introductionmentioning
confidence: 99%