RogerBlack
Senior Member
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- 902
My understanding is that calcium supplementation would do nothing. I may be wrong.
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Maybe. I have yet to read the full paper. What I think this might imply is a problem in intracellular ionized calcium regulation, which is ironic since I have been thinking about such things since about 2000 but have never been able to demonstrate it. Ionized calcium, and their opposition from cyclic AMP, represent important regulators of intracellular chemistry. A deficiency or imbalance will derange much of the biochemistry of the cell. The effects could be very broad at the intracellular chemistry level.Does this mean ME/CFS could be qualified as a calcium channelopathy?
Transient receptor potential (TRP) ion channels modulate ion entry in the cell plasma membrane, and are expressed differentially on tissues throughout the body.
Therefore, the objective of this study was to determine the effects of PregS on TRPM3, including CD69 and CD107a receptor expression in NK cells. Additionally, we investigated intracellular Ca2+mobilization and cytotoxic activity of NK cells after PregS treatment in HC and CFS/ME patients.
Increasing Ca2+ concentrations to activate the ERK signalling pathway may help to improve NK cell cytotoxicity in CFS/ME
Other TRP receptors, such as TRPM1, may possibly have a similar role in CFS/ME pathomechanism due to its sequence homology with TRPM3; however, further investigation is warranted
TRPM3 ion channels are expressed in various tissues, predominantly in sensory neurones, kidney, brain, pituitary gland and pancreas. While expressed ubiquitously in mammalian cells, the roles and functions of TRPM3 have yet to be determined in immune cells
A potential drug target.
Taking into account this unproven hypothesis:
... then we have a potential broad mechanism affecting many tissues under many circumstances. I think this is also a potential explanation for your question @Daisymay. They hypothesize its in many cell types, but this remains unproven.
Both. It depends on the problem. We have a lot to learn about this one. What we do know is that for many receptor subtypes there are a specific range of cells affected. However we do not know if this problem is specific to a subtype, or to TRPM receptors in general, or something in between.Thanks @alex3619. Do you know if in general, metabolic problems tend to occur in all cell types throughout the body or is it normal for them to be organ or cell type specific?
Maybe. I have yet to read the full paper. What I think this might imply is a problem in intracellular ionized calcium regulation, which is ironic since I have been thinking about such things since about 2000 but have never been able to demonstrate it. Ionized calcium, and their opposition from cyclic AMP, represent important regulators of intracellular chemistry. A deficiency or imbalance will derange much of the biochemistry of the cell. The effects could be very broad at the intracellular chemistry level.
One type of issue resulting in this would be a channelopathy, but I am unsure this is the only potential cause.