# Identification of key genes associated with muscle atrophy after spinal cord injury and experimental verification in rats

## TL;DR

This study identifies key genes linked to muscle atrophy after spinal cord injury in rats and validates their role through experiments.

## Contribution

The study identifies FOS and CCL2 as potential molecular targets for SCI-related muscle atrophy.

## Key findings

- 1007 differentially expressed genes were identified, with 533 upregulated and 474 downregulated.
- WGCNA analysis found a turquoise module of genes significantly associated with SCI-related muscle atrophy.
- FOS and CCL2 were highlighted as potential diagnostic or therapeutic targets for muscle atrophy after SCI.

## Abstract

Spinal cord injury (SCI) is a neurological disease with high morbidity and mortality. Post-SCI muscle atrophy is a cascade response to SCI, and failure to actively prevent its occurrence severely affects patients’ mobility and quality of life. Therefore, deeply exploring the correlation between muscle atrophy after SCI and the molecular regulation mechanism is of great significance.

Download GSE21497 expression profile data from the gene expression omnibus (GEO) database. Perform weighted gene co-expression network analysis (WGCNA) on the obtained differentially expressed genes (DEGs). Subsequently, we performed functional and pathway enrichment analyses of key modules. Construct a protein-protein interaction (PPI) network and screen core genes. Finally, the results were verified by real-time polymerase chain reaction(PCR).

A total of 1007 DEGs were obtained, including 533 upregulated genes and 474 downregulated genes. WGCNA analysis identified 161 turquoise modules of DEGs as key modules related to SCI. Functional enrichment analysis showed that these genes were mainly enriched in negative regulation of cellular process, cytosol, response to organic substance, endpoint system, extracellar region, peroxisome proliferators-activated receptors (PPARs) signaling, adherens junction signaling, and DNA replication signaling pathway.

FOS and CCL2 may be involved in the molecular pathophysiology of muscle atrophy after SCI, serving as potential targets for diagnosis or treatment of SCI-related muscle atrophy.