B-lymfocytt deplesjon og sykdomsmekanismer ved kronisk utmattelsessyndrom/ myalgisk encephalopati (ME/CFS)
It is in Norwegian, but page 26 and 28 are in English.
The hypothesis is about endothelial dysfunction in ME/CFS, and as you can see from page 28 nitric oxide (NO) production in the caveolae is of relevance.
I have written about Endothelial dysfunction in ME/CFS – and cytochrome CYP2C9, but to find out what is the disease mechanism in ME/CFS, I think we have to learn more about what is going on in the caveolae. Therefore I have searched for some articles about the caveolae and NO production. So, this is not about ME/CFS - this is basic knowledge about caveolae, nitric oxide and nitric oxide synthesis:
Regulation of eNOS in caveolae from: Nitric oxide signaling specificity — the heart of the problem
CAVEOLAE, CAVEOLIN AND CONTROL OF VASCULAR TONE: NITRIC OXIDE (NO) AND ENDOTHELIUM DERIVED HYPERPOLARIZING FACTOR (EDHF) REGULATION (Please, take a look at the figure at page 107).
Endothelium plays a crucial role in the regulation of cardiovascular homeostasis through the release of vasoactive factors. Two major actors controlling the vasomotor tone:Nitric oxide (NO) synthesis is catalysed by three isoforms of nitric oxide synthase (NOS) that have different tissue distributions: neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS)
Model for TRPC5-mediated feedback of Ca2+ and NO signaling in endothelial cells and attenuation of Ca2+ entry through TRPC6 by NO in smooth muscle cells
Endocytic trafficking in the subcellular localization and activity of eNOS: Vesicular Trafficking of Tyrosine Kinase Receptors and Associated Proteins in the Regulation of Signaling and Vascular Function
And we also need to look into the connection between nitric oxide and the mitochondria: