New Mouse Model Shows Autophagy as Potential New Factor in Fibromyalgia

New Mouse Model Shows Autophagy as Potential New Factor in Fibromyalgia

Researchers using a new mouse model found novel aspects of fibromyalgia disease connected to metabolic and molecular changes, including mitochondria damage and autophagy activation.

The study, “Fibromyalgia syndrome: metabolic and autophagic processes in intermittent cold stress mice,” was published in the journal Pharmacology Research & Perspectives.

To study the mechanisms of fibromyalgia syndrome, researchers have developed animal models with pharmacological influence on central nervous mediators such as serotonin, noradrenalin, or intramuscular injection of acid. Another model had stress‐induced hyperalgesia (abnormally heightened sensitivity to pain) and a new one had intermittent cold stress (ICS).

The ICS models had fibromyalgia‐like long‐lasting hyperalgesia and allodynia (central pain sensitization resulting from increased neuronal response). Like clinical fibromyalgia patients, the symptomatic pain in the mice could be resolved with antidepressants and gabapentin.

But a question remained whether ICS has an impact in other skeletal muscles features, particularly on metabolism, mitochondrial function, morphology, and cellular process such as autophagy (in which proteins and damaged organelles are naturally destroyed).

To find the answer, researchers analyzed the function of mitochondria and the autophagy pathway in ICS mice. The team recovered muscle and liver specimens from 36 mice and performed analysis of several molecular markers for metabolism alterations, muscle morphology changes, and mitochondrial and autophagy related markers.

Researchers observed that ICS induced a metabolic alteration characterized by reduction of ATP levels (cellular energy) in a mouse muscle cell line. ICS mice also showed lower levels of glycogen content in muscle and liver tissue. The changes were accompanied by morphological alterations of muscle cells, and with mitochondrial damage and autophagy activation.

The results suggest that the ICS mouse model is characterized by mitochondrial dysfunction, autophagy activation, and metabolic alterations and that some pathologic features described in the ICS mouse model are similar to human fibromyalgia syndrome.

Researchers concluded that more studies are required to investigate how the alterations contribute to fibromyalgia. The answers may lead to identifying potential new therapeutic options and establishing diagnostic markers for the disease.