ArticleJournal of orthopaedic translation2026
Mitochondrial metabolism restoration via Tramiprosate suppresses mitochondrial ROS-driven foamy macrophage senescence post spinal cord injury.
Article in Journal of orthopaedic translation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- ADSC-derived mitochondrial nanovesicles transplantation alleviates capsular fibrosis and inflammation and improves joint mobility in a rat model of adhesive capsulitis.Journal of orthopaedic translation · 2026Article
- Hypoxia-preconditioned mitochondrial transplantation multidirectionally modulates Schwann cell functions to repair peripheral nerve injury in rats.Journal of orthopaedic translation · 2026Article
- Integrating mechanistic research and emerging technologies to advance clinical translation in orthopaedics.Journal of orthopaedic translation · 2026Article
- Mitochondrial dysfunction and the regulatory cell death crosstalk network in chronic obstructive pulmonary disease: from oxidative stress mechanisms to targeted therapeutic strategies.Frontiers in immunology · 2026Review
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Authors and funding
12 authors.
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Abstract
Background: Myelin debris (MD) engulfment-induced foamy macrophage formation is a core neuropathology following spinal cord injury (SCI). The accumulation of these foamy macrophages within the injured foci sustains neuroinflammation, impeding long-term neuroregeneration and functional recovery. However, the mechanism underlying macrophage deterioration post-foaming remains elusive. Methods: MD-induced foamy macrophage and SCI model were used to investigated the role of Tramiprosate (TMP) Results: The current study reveals that lipid droplet-laden foamy macrophages exhibit mitochondrial dysfunction and a senescent phenotype, characterized by increased secretion of matrix metalloproteinases and proinflammatory cytokines. Restoring mitochondrial metabolism via TMP-via upregulation of Shmt2-inhibits mitochondrial reactive oxygen species (mtROS) and mitochondrial DNA (mtDNA) leakage. This reduces oxidative damage to nuclear DNA and suppresses the cyclic GMP-AMP synthase (cGAS)-mediated inflammatory response, thereby eliminating senescence in foamy macrophages. Conclusions: Our work demonstrates that TMP is a potential therapeutic agent targeting mitochondrial dysfunction-induced macrophage senescence post SCI. The Translational Potential of this Article: This study investigates the mechanisms underlying macrophage senescence following SCI and identifies TMP as a potential therapeutic agent to mitigate this process. Importantly, TMP is a taurine analogue with established blood-brain barrier permeability and a favorable safety profile in prior clinical investigations for neurodegenerative diseases. These characteristics support its potential treatment strategy for SCI.
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