Mitochondrial metabolism restoration via Tramiprosate suppresses mitochondrial ROS-driven foamy macrophage senescence post spinal cord injury - PubMed
2 days ago
- #Spinal Cord Injury
- #Mitochondrial Metabolism
- #Macrophage Senescence
- Mitochondrial metabolism restoration via Tramiprosate (TMP) suppresses mitochondrial ROS-driven foamy macrophage senescence post spinal cord injury (SCI).
- Foamy macrophages, formed due to myelin debris engulfment, sustain neuroinflammation and impede neuroregeneration after SCI.
- TMP restores mitochondrial metabolism by upregulating Shmt2, inhibiting mtROS and mtDNA leakage, reducing oxidative damage and suppressing cGAS-mediated inflammation.
- TMP shows potential as a therapeutic agent for SCI, with a favorable safety profile and blood-brain barrier permeability.
- The study highlights the role of mitochondrial dysfunction in macrophage senescence and identifies TMP as a promising treatment strategy.