#35904 Mitochondrial dysfunction as triggering in complex regional pain syndrome

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Background and Aims

Complex regional pain syndrome (CRPS) is characterized by being disproportionate to the triggering event; the associated characteristics are autonomic dysfunction, swelling of the zone of affection, and even changes in the skin, such as dystrophy and rigidity. The pathophysiology is still unknown; it has been mentioned as a multifactorial disorder, with an exaggerated immune response to the triggering event, abnormal vasomotor function, and even maladaptive neuroplasticity. This study aimed to evaluate the differently expressed genes (DEG) between 4 patients with complex regional pain syndrome vs. healthy controls and analyze the pathways intervening.

Methods

Material/Methods: The gene expression dataset GSE47603 was downloaded from the GEO database, and DEG obtained. The highest up-regulated genes were examined in the String platform for the protein-protein interaction (PPI) network.

Results

Results: 60 primary genes up-regulated were identified according to the Log2-fold change statistics. The network for the 60 genes was sub-selected in clusters in STRING, obtaining a network of 20 nodes, 24 edges, and a PPI enrichment p-value of 3.73e-11. The principal intervening pathways were mitochondrial ATP synthesis, the electron transport chain, and lysosome vesicle biogenesis.

Conclusions

We found a relevant participation of mitochondrial metabolism in the PPI network that has not been mentioned before as a pain onset in CRPS, but at the same time presence of pain has been reported in patients with mitochondrial disease, the essential role that it could play in the sudden development of pain in CRPS needs to be further analyzed.