Frontiers in Nutrition, 2023 · DOI: 10.3389/fnut.2023.1099143 · Published: March 3, 2023
Spinal cord injury (SCI) disrupts nerve connections to muscles, leading to muscle atrophy, which is worsened by factors like reduced activity, hormone changes, inflammation, and oxidative stress. This atrophy involves muscle cell death, protein breakdown, and fat buildup, hindering motor function recovery and affecting overall health. Research shows inflammation and oxidative stress are key drivers of muscle atrophy after SCI, involving multiple molecular pathways. While these pathways could be targets for clinical intervention, most studies are in early research stages. Current treatments mainly focus on rehabilitation training. This review examines the mechanisms of muscle atrophy after SCI, summarizing related cytokines and signaling pathways from recent studies, aiming to suggest new treatment ideas for clinical application.
Future therapeutic modalities may be explored and investigated at the cellular and molecular levels to optimize current clinical treatment options and improve the therapeutic effect of skeletal muscle atrophy after SCI, thus effectively promoting functional recovery after SCI.
A good nutritional intervention program may improve the treatment effect of SCI skeletal muscle atrophy and optimize the treatment plan. Glycine therapy may be a safe, effective and promising dietary treatment.
Combining exercise training with adjuvant therapies such as non-invasive transcutaneous spinal cord stimulation (tSCS), N-3 unsaturated fatty acids, and testosterone and androgen therapy can provide a better outcome.