ArticleJournal of cellular and molecular medicine2023
Therapeutic potential of melatonin in the intervertebral disc degeneration through inhibiting the ferroptosis of nucleus pulpous cells.
Article in Journal of cellular and molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Global trends and hotspots of macrophage-related research in intervertebral disc degeneration from 2005 to 2025: a bibliometric and visualized analysis.Frontiers in immunology · 2026Pooled it
- Ferroptosis in Spine-Related Diseases: Mechanistic Insights and Potential Therapeutic Targets.Cellular and molecular neurobiology · 2026Review
- Targeting Inflammatory Cell Death: A Strategy for Discogenic Pain Relief.Journal of pain research · 2026Review
- Melatonin Attenuates Spinal Cord Injury by Regulating Ferroptosis Through the Nrf2/HO-1/GPX4 Pathway.Molecular neurobiology · 2025Article
- Inhibition of ferroptosis in inflammatory macrophages alleviates intestinal injury in neonatal necrotizing enterocolitis.Cell death discovery · 2025Article
- Article
- 1,25(OH)₂D₃ inhibits ferroptosis in nucleus pulposus cells via VDR signaling to mitigate lumbar intervertebral disc degeneration.Scientific reports · 2025Article
- Mechanisms and Therapeutic Potential of GPX4 in Pain Modulation.Pain and therapy · 2025Review
- Role of macrophage in intervertebral disc degeneration.Bone research · 2025Review
- Ferroptosis and bone health: bridging the gap between mechanisms and therapy.Frontiers in immunology · 2025Review
- Progress of melatonin in the treatment of intervertebral disc degeneration.Frontiers in physiology · 2025Review
- Exploration and breakthrough in the mode of intervertebral disc cell death may lead to significant advances in treatments for intervertebral disc degeneration.Journal of orthopaedic surgery and research · 2024Review
- Targeting nucleus pulposus cell death in the treatment of intervertebral disc degeneration.JOR spine · 2024Review
- Identifying the protective effects of miR-874-3p/ATF3 axis in intervertebral disc degeneration by single-cell RNA sequencing and validation.Journal of cellular and molecular medicine · 2024Article
- Melatonin: a ferroptosis inhibitor with potential therapeutic efficacy for the post-COVID-19 trajectory of accelerated brain aging and neurodegeneration.Molecular neurodegeneration · 2024Review
- "Dictionary of immune responses" reveals the critical role of monocytes and the core target IRF7 in intervertebral disc degeneration.Frontiers in immunology · 2024Article
- Identification and validation of ferroptosis-related biomarkers in intervertebral disc degeneration.Frontiers in cell and developmental biology · 2024Article
- DNMT3a-mediated methylation of PPARγ promote intervertebral disc degeneration by regulating the NF-κB pathway.Journal of cellular and molecular medicine · 2024Article
- Targeting epigenetic and posttranslational modifications regulating ferroptosis for the treatment of diseases.Signal transduction and targeted therapy · 2023Review
- ACSL4 inhibition prevents macrophage ferroptosis and alleviates fibrosis in bleomycin-induced systemic sclerosis model.Arthritis research & therapy · 2023Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ferroptosis, a novel type of cell death mediated by the iron-dependent lipid peroxidation, contributes to the pathogenesis of the intervertebral disc degeneration (IDD). Increasing evidence demonstrated that melatonin (MLT) displayed the therapeutic potential to prevent the development of IDD. Current mechanistic study aims to explore whether the downregulation of ferroptosis contributes to the therapeutic capability of MLT in IDD. Current studies demonstrated that conditioned medium (CM) from the lipopolysaccharide (LPS)-stimulated macrophages caused a series of changes about IDD, including increased intracellular oxidative stress (increased reactive oxygen species and malondialdehyde levels, but decreased glutathione levels), upregulated expression of inflammation-associated factors (IL-1β, COX-2 and iNOS), increased expression of key matrix catabolic molecules (MMP-13, ADAMTS4 and ADAMTS5), reduced the expression of major matrix anabolic molecules (COL2A1 and ACAN), and increased ferroptosis (downregulated GPX4 and SLC7A11 levels, but upregulated ACSL4 and LPCAT3 levels) in nucleus pulposus (NP) cells. MLT could alleviate CM-induced NP cell injury in a dose-dependent manner. Moreover, the data substantiated that intercellular iron overload was involved in CM-induced ferroptosis in NP cells, and MLT treatment alleviated intercellular iron overload and protected NP cells against ferroptosis, and those protective effects of MLT in NP cells further attenuated with erastin and enhanced with ferrostatin-1(Fer-1). This study demonstrated that CM from the LPS-stimulated RAW264.7 macrophages promoted the NP cell injury. MLT alleviated the CM-induced NP cell injury partly through inhibiting ferroptosis. The findings support the role of ferroptosis in the pathogenesis of IDD, and suggest that MLT may serve as a potential therapeutic approach for clinical treatment of 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.