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The researchers found lowered intracellular calcium. Lowering it further (e.g. by blockage) is maybe not the right thing to do...
L-type calcium channels and TRPM3 are different (how exactly, please don't ask
).
As you know, in my case another calcium channel is affected, so that I start to think that many ways lead to Rome, i.e. different (let me call it) calcium channelopathies maybe lead to similar symptoms, maybe even to very similar pathomechanisms. Because if one part in the calcium signaling cascade is affected, the rest may be too.
This isn't known yet. It could be autoimmunity, it could be "mutated" channels, it could be something else (viruses?).
Not many human calcium channels can be researched, human NK cells seem to be suited (at least this is how I understood a researcher who explained to me the tests they will be doing on "my" calcium channel).
It would make sense to call a calcium channel that produces a dysfunctional calcium signal (and which leads to symptoms/disease) a "calcium channelopathy" , wouldn't it?