ArticleJOR spine2025
Phosphatidylcholine Ameliorates Palmitic Acid-Induced Lipotoxicity by Facilitating Endoplasmic Reticulum and Mitochondria Contacts in Intervertebral Disc Degeneration.
Article in JOR spine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Mitochondria‑associated endoplasmic reticulum membranes in degenerative musculoskeletal disorders: Mechanistic evidence and therapeutic perspectives (Review).Molecular medicine reports · 2026Review
- Betaine in Metabolic Dysfunction-Associated Steatotic Liver Disease: Mechanisms of Action and Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2026Review
- Article
- Phosphatidylethanolamine Alleviates Osteoarthritis Progression by Inhibiting Oxidative Stress-Induced Chondrocyte Ferroptosis in a Lysosomal-Dependent Manner.International journal of general medicine · 2026Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Intervertebral disc degeneration (IDD) is a prevalent musculoskeletal disorder with substantial socioeconomic impacts. Despite its high prevalence, the pathogenesis of IDD remains unclear, and effective pharmacological interventions are lacking. This study aimed to investigate metabolic alterations in IDD and explore potential therapeutic targets by analyzing lipotoxicity-related mechanisms in nucleus pulposus (NP) cells. Methods: Metabolomics and magnetic resonance spectroscopy were utilized to profile metabolic changes in NP tissues from advanced-stage IDD. Transcriptomics and metabolomics integration were performed to identify key regulatory pathways. In vitro experiments using human NP cells exposed to palmitic acid were conducted to evaluate endoplasmic reticulum (ER) stress, mitochondrial dysfunction, lipid droplet accumulation, and senescence. Phosphatidylcholine supplementation was tested for its ability to mitigate lipotoxicity, with ER-mitochondria interactions and mitochondrial oxidation capacity assessed as mechanistic endpoints. Results: Our findings revealed an abnormal lipotoxic condition in NP cells from advanced-stage IDD. Furthermore, we identified abnormal accumulation of triglycerides and palmitic acid in NP cells from IDD. The palmitic acid accumulation resulted in endoplasmic reticulum stress, mitochondrial damage, lipid droplet accumulation, and senescence of NP cells. By integrating transcriptomics and metabolomics analyses, we discovered that phosphatidylcholine plays a role in regulating palmitic acid-induced lipotoxicity. Notably, phosphatidylcholine level was found to be low in the endoplasmic reticulum and mitochondria of advanced-stage NP cells. Phosphatidylcholine treatment alleviated palmitic acid-induced lipid droplet accumulation and senescence of NP cells by modulating ER-mitochondria contacts and mitochondrial oxidation capacity. Conclusion: Phosphatidylcholine emerges as a potential therapeutic agent to counteract lipotoxic stress by modulating organelle interactions and mitochondrial function. These findings advance our understanding of IDD pathogenesis and provide a novel metabolic target for therapeutic development.
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