I hope I didn't get too many things wrong here: Cadherins are rod-shaped proteins that cross the cell membrane. One end is outside of the cell where it can interact with cadherins from other cells. The other end is inside and attached to beta-catenin which has a role in cell homeostasis (including glucose uptake). Cadherins are important for cells to maintain the right distance from each other. Cells form attachments to other cells. The role of the cadherins is not to provide structural integrity to these attachments but guide the process so that it comes out right (in terms of distance, position, cell type, etc). If cells are too tightly attached to each other it could lead to poor nutrient uptake because there isn't enough space between cells for extracellular fluids. That seems like a straightforward way to make a connection between abnormalities in cadherins and related cellular pathways and components to the reduced peripheral blood flow that researcher suspect is present in ME/CFS. The published studies do show increased expression of cadherins and related pathways which is hard to interpret but doesn't seem inconsistent with this idea.
Perfusion typically refers to blood flow across a capillary bed, rather than cross membrane transport of molecules. But caherins are involved in cell adhesion and hypothetically, abnormalities could disrupt the normal function of cellular junctions. The following articles discuss various paracellular transport pathways. https://en.wikipedia.org/wiki/Adherens_junction https://en.wikipedia.org/wiki/Gap_junction https://en.wikipedia.org/wiki/Tight_junction But I don't think it would be as simple as "poor nutrient uptake due to adhesions being too tight". Much molecular transport is through cellular membranes rather than paracellular pathways, none of which explains poor perfusion.
No idea on this but a thought occurred; If the purpose of these whatsits is to maintain the correct distance between cells, and the level of various transmitters is important in intercellular signalling, then surely the distance between cells must be important for this signalling. That is too close and the levels would be higher than the transmitting cell 'intended' and too far the levels would be lower. This could really muck things up, unless the transmission system depends on being saturated to get a message across. So, nothing to do with cellular feeding or stability, or anything else, needed to explain a problem if these whatsits aren't right - simple/basic intercellular communication could go haywire.
It turns out cadherins and integrins play a role in the body's response to upright posture. If I understand all this right, a problem with these or more generally cell-cell adhesion could plausibly lead to orthostatic intolerance. And the body might respond to that problem by dumping lots of vasoconstricting substances into the blood in an attempt to get the smooth muscles of the arteries to contract more and prevent blood pooling. N-Cadherin and Integrin Blockade Inhibit Arteriolar Myogenic Reactivity but not Pressure-Induced Increases in Intracellular Ca2+ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3059933/ @Jonathan Edwards maybe this is where your "signalling problem" is?
