Effects of Advancement on Biomechanics and Biology on Active Performance

Gokay, Nevzat Selim; Kon, Elizaveta; Yılmaz, İbrahim; Gökçe, Alper

doi:10.1007/978-3-642-36801-1_275-1

Cited by 1 publication

(2 citation statements)

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“…2). All three isoforms of NOS are detected in chondrocytes although most studies have focused on iNOS which is upregulated by pro-inflammatory factors [61][62][63]. In the context of cartilage, studies have suggested that •NO can promote chondrocyte death via apoptosis [61], while others have shown that •NO alone does not cause chondrocyte death but rather NO induces apoptosis when it reacts with O 2 • to form the highly oxidizing ONOO- [64].…”

Section: Nitric Oxidementioning

confidence: 99%

“…The relative levels of •NO produced by nNOS in chondrocytes is not known, although nNOS expression was noted in normal chondrocytes while iNOS was suggested to be the dominant isoform in OA chondrocytes [63,75]. One study found that chemical nNOS inhibition promoted cartilage restoration in a rat model of cartilage damage whereas iNOS inhibition had no effect [62]. Further work is needed to better define the role of nNOS in cartilage homeostasis.…”

Section: Nitric Oxidementioning

confidence: 99%

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Reactive oxygen species, aging and articular cartilage homeostasis

Bolduc

Collins

Loeser

2019

Free Radical Biology and Medicine

407

286

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Chondrocytes are responsible for the maintenance of the articular cartilage. A loss of homeostasis in cartilage contributes to the development of osteoarthritis (OA) when the synthetic capacity of chondrocytes is overwhelmed by processes that promote matrix degradation. There is evidence for an age-related imbalance in reactive oxygen species (ROS) production relative to the anti-oxidant capacity of chondrocytes that plays a role in cartilage degradation as well as chondrocyte cell death. The ROS produced by chondrocytes that have received the most attention include superoxide, hydrogen peroxide, the reactive nitrogen species nitric oxide, and the nitric oxide derived product peroxynitrite. Excess levels of these ROS not only cause oxidative-damage but, perhaps more importantly, cause a disruption in cell signaling pathways that are redox-regulated, including Akt and MAP kinase signaling. Age-related mitochondrial dysfunction and reduced activity of the mitochondrial superoxide dismutase (SOD2) are associated with an increase in mitochondrial-derived ROS and are in part responsible for the increase in chondrocyte ROS with age. Peroxiredoxins (Prxs) are a key family of peroxidases responsible for removal of HO, as well as for regulating redox-signaling events. Prxs are inactivated by hyperoxidation. An age-related increase in chondrocyte Prx hyperoxidation and an increase in OA cartilage has been noted. The finding in mice that deletion of SOD2 or the anti-oxidant gene transcriptional regulator nuclear factor-erythroid 2- related factor (Nrf2) result in more severe OA, while overexpression or treatment with mitochondrial targeted anti-oxidants reduces OA, further support a role for excessive ROS in the pathogenesis of OA. Therefore, new therapeutic strategies targeting specific anti-oxidant systems including mitochondrial ROS may be of value in reducing the progression of age-related OA.

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Section: Nitric Oxidementioning

confidence: 99%

Section: Nitric Oxidementioning

confidence: 99%