Molecular laser biotechnology

Grishko, V.P.; Grishko, Victor I.; Glick, Bernard R.

doi:10.1016/s0734-9750(99)00015-4

Cited by 10 publications

(1 citation statement)

References 109 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, deletion of SOD1 in the kidneys of mice has been shown to enhance DNA oxidative damage, upregulate markers of cellular senescence and increase production of senescence-associated secretory proteins, when compared to the kidneys of wild type mice [110], which suggests a possible connection between oxidative stress, antioxidant function and senescence [110]. Increased age-related and oxidative stress-induced telomere shortening [111,112] DNA damage [101,113] and mitochondrial dysfunction [6,11] are documented in OA tissues. Since these stressors can all induce the senescent phenotype, a role for oxidative stress-induced senescence in OA appears plausible and could represent a novel and exciting avenue for OA research going forwards.…”

Section: Cellular Senescence In Aging and Oamentioning

confidence: 99%

Reactive oxygen species, aging and articular cartilage homeostasis

Bolduc

Collins

Loeser

2019

Free Radical Biology and Medicine

409

286

View full text Add to dashboard Cite

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.

show abstract