Association between dystrophin, focal adhesion and muscle fatigability - discussion thread

(I apologise if this seems to be a little obscure).

Animal models suggest a relationship between dystrophin and muscle fibre fatiguability.

Hyperhomocysteinemia associated skeletal muscle weakness involves mitochondrial dysfunction and epigenetic modifications
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4372482/

Correlation of dystrophin–glycoprotein complex and focal adhesion complex with myosin heavy chain isoforms in rat skeletal muscle
https://pubmed.ncbi.nlm.nih.gov/19040708/

Note that. Dystrophin-knock out mice are used as an animal model of Duchenne muscular dystrophy, which is a genetic disorder caused by a SNP in the dystrophin gene.

Also notably, that Urocortins are often used in these animal models to (partially) restore motorfunction such as:
Recovery of Respiratory Function in MDX Mice Co-Treated With Neutralizing interleukin-6 Receptor Antibodies and urocortin-2
https://pubmed.ncbi.nlm.nih.gov/30160301/

Which curiously has some relevance to the Cortene trial.

Now ME or CFS are not muscular dystrophies, with an absence of excess creatine kinase or muscle breakdown products detected in most patients. However that isn't to say that issues couldn't be caused by sensitisation of type 3 sensory fibres due to mechanoreceptor stimulation, perhaps during the post-exercise repair phase due to focal adhesion dysfunction. Alternatively, this dysfunction of focal adhesion could lead to endothelial dysfunction.

Mechanotransduction in striated muscle via focal adhesion kinase
https://hal.archives-ouvertes.fr/hal-00187530v2/document

Gene Expression Profile Exploration of a Large Dataset on Chronic Fatigue Syndrome
https://pubmed.ncbi.nlm.nih.gov/16610953/