ArticleScience translational medicine2023
Lesion level-dependent systemic muscle wasting after spinal cord injury is mediated by glucocorticoid signaling in mice.
Article in Science translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- A biodegradable piezoelectric vertebral implant for programmable electro-neuromodulation in spinal cord injury.Science advances · 2026Article
- Spinal cord tissueoid transplantation combined with tail nerve electrical stimulation promotes the voluntary movement of paralyzed hindlimbs in rats with transected spinal cord injury.Materials today. Bio · 2026Article
- Disruption of the spinal cord-gut axis alters microbial dynamics and carbohydrate cross-feeding in the gut.Communications biology · 2026Article
- Mechanisms of protein degradation in atrophying muscles: What have we learned during the past decade?The Journal of biological chemistry · 2026Review
- Lesion level and severity acutely influence metabolomic profiles in spinal cord injury.Journal of neuropathology and experimental neurology · 2026Article
- Nouveau benzo-mimetics of 17R-Resolvin D2 are potent resolution agonists for inflammation.iScience · 2025Article
- Unveiling the Significance of Peroxiredoxin 6 in Central Nervous System Disorders.Antioxidants (Basel, Switzerland) · 2024Review
- Effect of body mass index on survival after spinal cord injury.Frontiers in neurology · 2023Article
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
An incomplete mechanistic understanding of skeletal muscle wasting early after spinal cord injury (SCI) precludes targeted molecular interventions. Here, we demonstrated systemic wasting that also affected innervated nonparalyzed (supralesional) muscles and emerged within 1 week after experimental SCI in mice. Systemic muscle wasting caused muscle weakness, affected fast type 2 myofibers preferentially, and became exacerbated after high (T3) compared with low (T9) thoracic paraplegia, indicating lesion level-dependent ("neurogenic") mechanisms. The wasting of nonparalyzed muscle and its rapid onset and severity beyond what can be explained by disuse implied unknown systemic drivers. Muscle transcriptome and biochemical analysis revealed a glucocorticoid-mediated catabolic signature early after T3 SCI. SCI-induced systemic muscle wasting was mitigated by (i) endogenous glucocorticoid ablation (adrenalectomy) and (ii) pharmacological glucocorticoid receptor (GR) blockade and was (iii) completely prevented after T3 relative to T9 SCI by genetic muscle-specific GR deletion. These results suggest that neurogenic hypercortisolism contributes to a rapid systemic and functionally relevant muscle wasting syndrome early after paraplegic SCI in mice.
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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 Socratic graph.