title: ROS: Crucial Intermediators in the Pathogenesis of Intervertebral Disc Degeneration.
abstract: Excessive reactive oxygen species (ROS) generation in degenerative intervertebral disc (IVD) indicates the contribution of oxidative stress to IVD degeneration (IDD), giving a novel insight into the pathogenesis of IDD. ROS are crucial intermediators in the signaling network of disc cells. They regulate the matrix metabolism, proinflammatory phenotype, apoptosis, autophagy, and senescence of disc cells. Oxidative stress not only reinforces matrix degradation and inflammation, but also promotes the decrease in the number of viable and functional cells in the microenvironment of IVDs. Moreover, ROS modify matrix proteins in IVDs to cause oxidative damage of disc extracellular matrix, impairing the mechanical function of IVDs. Consequently, the progression of IDD is accelerated. Therefore, a therapeutic strategy targeting oxidative stress would provide a novel perspective for IDD treatment. Various antioxidants have been proposed as effective drugs for IDD treatment. Antioxidant supplementation suppresses ROS production in disc cells to promote the matrix synthesis of disc cells and to prevent disc cells from death and senescence in vitro. However, there is not enough in vivo evidence to support the efficiency of antioxidant supplementation to retard the process of IDD. Further investigations based on in vivo and clinical studies will be required to develop effective antioxidative therapies for IDD.
authors.affiliation: Department of Orthopedics, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China.
authors.forename: Chencheng
authors.identifier: 0000-0002-9393-304X
authors.initials: C
authors.lastname: Feng
authors.affiliation: Department of Orthopedics, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China.
authors.forename: Minghui
authors.initials: M
authors.lastname: Yang
authors.affiliation: Department of Orthopedics, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China.
authors.forename: Minghong
authors.initials: M
authors.lastname: Lan
authors.affiliation: Department of Orthopedics, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China.
authors.forename: Chang
authors.initials: C
authors.lastname: Liu
authors.affiliation: Department of Orthopedics, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China.
authors.forename: Yang
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Department of Orthopedics, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China.
authors.forename: Bo
authors.initials: B
authors.lastname: Huang
authors.affiliation: Department of Orthopedics, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China.
authors.forename: Huan
authors.identifier: 0000-0002-5519-7336
authors.initials: H
authors.lastname: Liu
authors.affiliation: Department of Orthopedics, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China.
authors.forename: Yue
authors.identifier: 0000-0001-7102-6484
authors.initials: Y
authors.lastname: Zhou
mesh_terms: D060833:Cellular Microenvironment; D006706:Homeostasis; D006801:Humans; D007403:Intervertebral Disc / Q000503:physiopathology*; D055959:Intervertebral Disc Degeneration / Q000503:physiopathology*; D010084:Oxidation-Reduction; D017382:Reactive Oxygen Species / Q000378:metabolism*
chemical_list: D017382:Reactive Oxygen Species