ArticleCell proliferation2020
The mitochondria-targeted anti-oxidant MitoQ protects against intervertebral disc degeneration by ameliorating mitochondrial dysfunction and redox imbalance.
Article in Cell proliferation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
134 citing papers in PubMed, 192 citations in OpenAlex.
- A pilot double-blind, placebo-controlled, randomized clinical trial of MitoQ in the treatment of septic shock: evaluating its effects on clinical outcomes and oxidative stress biomarker.Naunyn-Schmiedeberg's archives of pharmacology · 2026Trial
- Persistent ZnAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- CBX3 aggravates nucleus pulposus cell apoptosis and extracellular matrix degradation in vitro via repressing SESN2-mediated mitophagy in an H3K9me3-dependent manner.Molecular biology reports · 2026Article
- Ergothioneine-Derived Carbon Dot Nanozymes Alleviate the Oxidative Stress Microenvironment to Delay Intervertebral Disc Degeneration.Antioxidants (Basel, Switzerland) · 2026Article
- Targeting AMPK signaling in nucleus pulposus cells ameliorates spaceflight microgravity-induced intervertebral disc degeneration.Cell death and differentiation · 2026Article
- Cortistatin as a modulator of inflammatory and mitochondrial dysfunction in Huntington´s disease.Journal of neuroinflammation · 2026Article
- A pH‑responsive hydrogel delivering ISOC1 modRNA attenuates disc degeneration by promoting BIRC6‑mediated MYC degradation and inhibiting SBSN expression.Journal of nanobiotechnology · 2026Article
- Semaglutide targets muscle mitochondria to regulate glutamine metabolism and treat osteoarthritis.iScience · 2026Article
- Edaravone-based precision antioxidative therapy alleviates intervertebral disc degeneration via the Nrf2/Aldh3a1 axis.Materials today. Bio · 2026Article
- Ubiquitination in intervertebral disc degeneration: from mechanisms to potential therapeutic strategies.Journal of orthopaedic translation · 2026Review
- Current Perspective on Orthobiology Applications for the Treatment of Intervertebral Disc Degeneration (IDD)-A Narrative Review.Medicina (Kaunas, Lithuania) · 2026Review
- Mitochondria-driven ferroptosis in intervertebral disc degeneration: A novel target in age-related spinal diseases (Review).Experimental and therapeutic medicine · 2026Review
- Article
- Adapt, Mitigate, and Target: The Role of Oxidative Stress in Intervertebral Disc Homeostasis and Disc Degeneration.Neurospine · 2026Review
- Proteomic analysis identifies distinct signaling pathways in lumbar intervertebral disc degeneration between type-2 diabetic and non-diabetic patients.Scientific reports · 2026Article
- Exercise modulates redox homeostasis in cardiovascular and metabolic diseases: from bench to clinic.Cardiovascular diabetology · 2026Review
- HACE1 alleviates intervertebral disc degeneration by inhibiting ferroptosis in nucleus pulposus cells.Scientific reports · 2026Article
- Targeting mitochondrial oxidative stress: A novel therapeutic strategy for degenerative joint diseases (Review).Biomedical reports · 2026Review
- Metabolic reprogramming in intervertebral disc degeneration: mechanisms and therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Multi-Omics Bioinformatic Analyses Linking LOXL4 with Spondylolisthesis.Orthopedic research and reviews · 2026Article
74 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveMitochondrial dysfunction, oxidative stress and nucleus pulposus (NP) cell apoptosis are important contributors to the development and pathogenesis of intervertebral disc degeneration (IDD). Here, we comprehensively evaluated the effects of mitochondrial dynamics, mitophagic flux and Nrf2 signalling on the mitochondrial quality control, ROS production and NP cell survival in in vitro and ex vivo compression models of IDD and explored the effects of the mitochondria-targeted anti-oxidant MitoQ and its mechanism. MATERIAL AND
methodsHuman NP cells were exposed to mechanical compression to mimic pathological conditions.
resultsCompression promoted oxidative stress, mitochondrial dysfunction and NP cell apoptosis. Mechanistically, compression disrupted the mitochondrial fission/fusion balance, inducing fatal fission. Concomitantly, PINK1/Parkin-mediated mitophagy was activated, whereas mitophagic flux was blocked. Nrf2 anti-oxidant pathway was insufficiently activated. These caused the damaged mitochondria accumulation and persistent oxidative damage. Moreover, MitoQ restored the mitochondrial dynamics balance, alleviated the impairment of mitophagosome-lysosome fusion and lysosomal function and enhanced the Nrf2 activity. Consequently, damaged mitochondria were eliminated, redox balance was improved, and cell survival increased. Additionally, MitoQ alleviated IDD in an ex vivo rat compression model.
conclusionsThese findings suggest that comodulation of mitochondrial dynamics, mitophagic flux and Nrf2 signalling alleviates sustained mitochondrial dysfunction and oxidative stress and represents a promising therapeutic strategy for IDD; furthermore, our results provide evidence that MitoQ might serve as an effective therapeutic agent for this disorder.
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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.