ReviewOxidative medicine and cellular longevity2022
Oxidative Stress and Intervertebral Disc Degeneration: Pathophysiology, Signaling Pathway, and Therapy.
Review in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed.
- Biomaterials for intervertebral disc regeneration: Niche reprogramming, precision therapeutics, and structural reconstruction.Bioactive materials · 2027Review
- Antioxidant Nanotherapies for Intervertebral Disk Degeneration: Progress and Prospects.Antioxidants (Basel, Switzerland) · 2026Review
- A manganese-luteolin co-loaded antioxidant hydrogel for synergistic alleviation of oxidative stress and immunomodulation in intervertebral disc degeneration.Materials today. Bio · 2026Article
- A continuous DNA repairing system for alleviating intervertebral disc degeneration.Journal of nanobiotechnology · 2026Article
- Gingerol-loaded hollow manganese dioxide nanoparticles attenuate intervertebral disc oxidative stress.RSC advances · 2026Article
- Article
- A ROS and pH dual - responsive hydrogel-nanoparticle system restores intervertebral disc and alleviates related pain by modulating senescence and panoptosis of nucleus pulposus cells.Materials today. Bio · 2026Article
- Obesity and oxidative stress: potential mechanisms in endometrial disorders.Frontiers in endocrinology · 2026Review
- Region-dependent expression and function of integrin α5β1 in protecting against disc degenerationFrontiers in bioengineering and biotechnology · 2026Article
- Nystose treats intervertebral disc degeneration via the Nrf2 axis: a focus on oxidative stress and ferroptosis.Frontiers in pharmacology · 2026Article
- Antioxidant biomaterials in intervertebral disc regeneration: current status and future clinical translation.Frontiers in bioengineering and biotechnology · 2026Review
- ASIC1a Promotes nucleus pulposus derived stem cells apoptosis through modulation of SIRT3-dependent mitochondrial redox homeostasis in intervertebral disc degeneration.Redox report : communications in free radical research · 2025Article
- Immunohistochemical analysis to detect a molecular signature in intervertebral disc degeneration.Histochemistry and cell biology · 2025Article
- Histone modifications: Unveiling the epigenetic enigma of degenerative skeletal diseases.Journal of orthopaedic translation · 2025Review
- Understanding the Microenvironment of Intervertebral Disc Degeneration: A Comprehensive Review of Pathophysiological Insights and Therapeutic Implications.International journal of molecular sciences · 2025Review
- Tie2-mediated CBL ubiquitination of EGFR underlies ultrasound-responsive silk fibroin/graphene oxide hydrogel-troxerutin therapy for intervertebral disc degeneration.Materials today. Bio · 2025Article
- Postoperative Changes in Hematological, Biochemical, and Redox Status Parameters in Spinal Osteoarthritis Patients Undergoing Spinal Decompression and Stabilization Surgery.Journal of clinical medicine · 2025Article
- Bioactive Therapies for Degenerative Disc Disease: Challenges and Innovations.World neurosurgery · 2025Article
- NJournal of orthopaedic translation · 2025Review
- Apoptotic Pathway in Intervertebral Disc Degeneration: From Molecular Pathways to Clinical Interventions.Diagnostics (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intervertebral disc degeneration (IDD), characterized as decreased proteoglycan content, ossification of endplate, and decreased intervertebral height, is one of the major reasons of low back pain, which seriously affects the quality of life and also brings heavy economic burden. However, the mechanisms leading to IDD and its therapeutic targets have not been fully elucidated. Oxidative stress refers to the imbalance between oxidation and antioxidant systems, between too many products of reactive oxygen species (ROS) and the insufficient scavenging function. Excessive ROS can damage cell lipids, nucleic acids and proteins, which has been proved to be related to the development of a variety of diseases. In recent years, an increasing number of studies have reported that oxidative stress is involved in the pathological process of IDD. Excessive ROS can accelerate the IDD process via inducing the pathological activities, such as inflammation, apoptosis, and senescence. In this review, we focused on pathophysiology and molecular mechanisms of oxidative stress-induced IDD. Moreover, the present review also summarized the possible ideas for the future therapy strategies of oxidative stress-related IDD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.