ROS/oxidative stress signaling in osteoarthritis

被引：768

作者：

Lepetsos, Panagiotis ^{[1
]}

Papavassiliou, Athanasios G. ^{[2
]}

机构：

[1] Natl & Kapodistrian Univ Athens, KAT Hosp, Sch Med, Dept Trauma & Orthopaed 4, Athens 14561, Greece

[2] Natl & Kapodistrian Univ Athens, Sch Med, Dept Biol Chem, 75 M Asias St, Athens 11527, Greece

来源：

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2016年 / 1862卷 / 04期

关键词：

Osteoarthritis; Oxidative stress; Chondrocytes; Reactive oxygen species; NO; Cartilage; NITRIC-OXIDE SYNTHASE; NF-KAPPA-B; HUMAN ARTICULAR CHONDROCYTES; LOW-DENSITY-LIPOPROTEIN; GLYCATION END-PRODUCTS; INDUCED CELL-DEATH; EXTRACELLULAR-SUPEROXIDE DISMUTASE; PROSTAGLANDIN E-2 PRODUCTION; MITOCHONDRIAL RESPIRATORY ACTIVITY; CARTILAGE PROTEOGLYCAN SYNTHESIS;

D O I：

10.1016/j.bbadis.2016.01.003

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Osteoarthritis is the most common joint disorder with increasing prevalence due to aging of the population. Its multi-factorial etiology includes oxidative stress and the overproduction of reactive oxygen species, which regulate intracellular signaling processes, chondrocyte senescence and apoptosis, extracellular matrix synthesis and degradation along with synovial inflammation and dysfunction of the subchondral bone. As disease-modifying drugs for osteoarthritis are rare, targeting the complex oxidative stress signaling pathways would offer a valuable perspective for exploration of potential therapeutic strategies in the treatment of this devastating disease. (C) 2016 Elsevier B.V. All rights reserved.

引用

页码：576 / 591

页数：16

共 341 条

[1]

Bioenergetics and the formation of mitochondrial reactive oxygen species [J].