HMN 2026: How Chain reaction in cells may be driving low energy in ME/CFS patients

Griffith University researchers have identified a key immune cell dysfunction in people with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), offering new clues about the condition.

The study addressed a critical question: Are the mitochondrial deficits reported by other researchers a downstream consequence of the ion-channel and calcium abnormalities previously identified?

Lead author Ph.D. candidate Chandi Magawa and the research team from Griffith’s National Center for Neuroimmunology and Emerging Diseases (NCNED) used advanced live-cell imaging to observe TRPM3-dependent calcium movement into mitochondria in real time.

The paper “Deficient TRPM3-linked mitochondrial Ca²⁺ influx in natural killer cells associated with myalgic encephalomyelitis/chronic fatigue syndrome” has been published in BMC Immunology.

“We found a significant TRPM3-calcium pathway dysfunction in ME/CFS, resulting in impaired calcium entry into mitochondria, a region of the cell responsible for energy production,” she said.

“It explains how reduced calcium entry into mitochondria may impair immune cell function and energy production, effectively triggering a chain reaction in the body.”

Dr. Natalie Eaton-Fitch said ME/CFS was a serious and complex condition for which there was no cure or treatment.

“The latest data from the Australian Institute of Health and Welfare estimates 219,000 Australians are living with the illness,” she said.

Symptoms included profound, persistent exhaustion; post-exertional malaise; pain; cognitive difficulties; dizziness; temperature instability; and sensory sensitivity, which could severely restrict day-to-day functioning, education, employment and social participation.

Professor Sonya Marshall-Gradisnik, NCNED director, said the study helped explain the underlying biological dysfunction, moving the condition further away from being misunderstood or dismissed.

“This research could contribute toward new diagnostic biomarkers and therapies focusing on ion channel dysfunction or calcium signaling,” Marshall-Gradisnik said.

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