2017
DOI: 10.1007/s00011-017-1121-8
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The interrelation of osteoarthritis and diabetes mellitus: considering the potential role of interleukin-10 and in vitro models for further analysis

Abstract: Future development of versatile micro-scaled in vitro models such as combining DM and OA on chip could allow the identification of common pathogenetic pathways and might help to develop novel therapeutic strategies.

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Cited by 22 publications
(31 citation statements)
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“…Low IL-10 but high pro-inflammatory cytokine IL-6 levels were associated with higher risks for lumbar OA in postmenopausal woman [20]. IL-10 provides an inhibitory effect on IL-1β and TNFα expression, on synthesis of matrix metalloproteinases (MMPs) as well as on secretion of prostaglandin E 2 (PGE 2 ) [12,14,17] which may result in protecting articular cartilage from the degenerative processes [21,22]. It stabilized the specific phenotype of chondrocytes, protects them from cell death and ECM degradation in response to mechanical injury [23,24].…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…Low IL-10 but high pro-inflammatory cytokine IL-6 levels were associated with higher risks for lumbar OA in postmenopausal woman [20]. IL-10 provides an inhibitory effect on IL-1β and TNFα expression, on synthesis of matrix metalloproteinases (MMPs) as well as on secretion of prostaglandin E 2 (PGE 2 ) [12,14,17] which may result in protecting articular cartilage from the degenerative processes [21,22]. It stabilized the specific phenotype of chondrocytes, protects them from cell death and ECM degradation in response to mechanical injury [23,24].…”
Section: Introductionmentioning
confidence: 99%
“…It stabilized the specific phenotype of chondrocytes, protects them from cell death and ECM degradation in response to mechanical injury [23,24]. However, so far, little information about the role of IL-10 and its mechanism of action in healthy and in OA cartilage under the conditions of hyperglycemia (HG) is available [22].…”
Section: Introductionmentioning
confidence: 99%
“…Saxagliptin, a novel dipeptidyl peptidase IV (DPP-4) inhibitor, suppresses the degradation of type II collagen in primary human chondrocytes by decreasing MMP, ADAMTS, and ROS production and increasing glutathione levels mediated by p38/NFkB pathway [142]. Metformin, the most commonly used antidiabetic drug, reduced inflammation, decreased the number of T helper 17 ( 17) cells, and increased the number of regulatory T (Treg) cells in a mouse model of collagen-induced arthritis [143]. erefore, it was reasonable to conclude that antidiabetic medications attenuate the deleterious effects of DM in patients with OA, and this action halts disease progression [144].…”
Section: Repurposing Of Antidiabetic Agents For the Treatment Ofmentioning
confidence: 99%
“…ese effects are attributable to the release of increased quantities of proinflammatory mediators, such as tumour necrosis factor (TNF)α, interleukin (IL)-6, and IL-1 from adipocytes in individuals with obesity. ese agents are known to trigger systemic low-grade inflammation in patients with both OA and TD [17].…”
Section: Introductionmentioning
confidence: 99%
“…Metabolic OA prevalence is highest in developed countries, where the incidence of obesity progressively increases due to a sedentary lifestyle, low levels of physical activity, and high-caloric diet [8]. The pathogenesis of metabolic OA has been linked to several features of the metabolic syndrome, such as central obesity, insulin resistance and dyslipidemia [2,9,10]. Even though the association between OA and metabolic stress is demonstrated by many studies, the underlying pathophysiologic mechanisms are still vague.…”
Section: Introductionmentioning
confidence: 99%