A faulty ion channel is linked to the exhaustion of ME/CFS

Griffith University researchers tie ME/CFS fatigue to a malfunctioning calcium pathway, but the study is small and early.

Researchers at Griffith University in Australia have identified a faulty cellular pathway that may help explain the exhaustion of ME/CFS. The ion channel TRPM3 appears to malfunction in natural killer white blood cells, disrupting the movement of calcium into mitochondria. The study, authored by Magawa et al., used live-cell imaging of natural killer cells from 10 people with ME/CFS and 10 healthy controls.

ME/CFS cells showed significantly reduced TRPM3-dependent calcium movement into cell fluid and mitochondria compared with controls. After calcium stores were depleted and restored, mitochondrial calcium influx was actually higher in the patient cells. TRPM3 is present not only in immune cells but in tissues across the nervous, gastrointestinal, cardiovascular, and musculoskeletal systems, which may hint at the disease's broad reach.

ME/CFS currently has no cure or approved treatment, so a concrete molecular target matters. The researchers note that prior work showed the drug naltrexone can restore TRPM3 activity in these cells, and a clinical trial is underway. A validated biomarker could also eventually support diagnosis of a condition that has long been hard to pin down.

The honest limits are large. The cohort is just 10 patients and 10 controls, ATP output was not directly measured so downstream energy effects remain untested, and the researchers caution the finding does not prove TRPM3 dysfunction causes all mitochondrial problems in ME/CFS. Any biomarker would need validation across larger cohorts and other fatigue conditions before clinical use.

Source: New Atlas