Despite the severity of symptoms and the discovery of numerous cardiovascular, microvascular and muscular abnormalities in scientific studies, no specific biomarker for ME/CFS has been found to date. However, new research shows a dysfunction of the Transient Receptor Potential Melastatin 3 (TRPM3) channel in natural killer cells (NK cells) of ME/CFS patients, characterized by reduced calcium influx. This dysfunction has also been observed in patients with post-Covid syndrome.
TRPM3 dysfunction plays a central role in the pathophysiology of ME/CFS at three key levels: in natural killer cells, sensory nerve fibers, and the brain. This dysfunction may contribute to the immunological disturbances, muscle dysfunction, and neurological symptoms seen in ME/CFS and PCS.
Given the different splice variants of the TRPM3 channel that strongly influence channel properties, it is important to investigate whether specific variants contribute to TRPM3 dysfunction and act as significant risk factors for the development of ME/CFS.
Treating TRPM3 dysfunction in small nerve fibers and the brain with low-dose naltrexone (LDN) may better explain the clinical efficacy of LDN in ME/CFS than targeting TRPM3 function in natural killer cells alone.
Source: Link.springer.com