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Updated: Apr 30, 2026

Evaluating the Role of Mitochondrial Function in Cancer-related Fatigue
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Mitochondria-Related Genome-Wide Mendelian Randomization Identifies Putatively Genes for Chronic Fatigue.

Zehan Zhang1, Zhuoyang Xiao1, Heting Mei2

  • 1School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Fangshan District, Beijing, China.

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|April 29, 2026
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Summary

This study identifies AKAP10 and MTHFD1L as key mitochondrial genes linked to chronic fatigue. Repurposed drugs targeting these genes show potential for new fatigue treatments.

Keywords:
Bayesian colocalizationChronic fatigueMitochondrionPhenome-wide association studySummary-data-based Mendelian randomization

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Area of Science:

  • Genetics
  • Mitochondrial Biology
  • Pharmacology

Background:

  • Chronic fatigue is a complex symptom associated with mitochondrial dysfunction.
  • Genetic underpinnings of chronic fatigue, particularly involving mitochondria, remain incompletely understood.
  • Identifying specific genes and therapeutic targets is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate mitochondrial-related genes causally associated with chronic fatigue.
  • To explore AKAP10 and MTHFD1L as potential therapeutic targets for chronic fatigue.
  • To evaluate the potential of repurposed drugs for treating chronic fatigue based on identified gene targets.

Main Methods:

  • Summary-data-based Mendelian randomization (SMR) and Bayesian colocalization analyses were performed using large-scale genetic datasets (eQTL and GWAS).
  • Mitochondrial genes were identified from the MitoCarta3.0 database.
  • Two-sample Mendelian randomization (TSMR), gene expression analysis in rat fatigue models, drug-gene interaction screening (DSigDB, DrugBank), molecular docking, and phenome-wide association studies (PheWAS) were utilized.

Main Results:

  • SMR and colocalization analyses identified nine mitochondrial genes, with AKAP10 and MTHFD1L showing robust causal links to chronic fatigue.
  • TSMR analysis confirmed significant causal relationships for AKAP10 and MTHFD1L with chronic fatigue.
  • Gene expression data from rat models showed significantly upregulated Akap10 and Mthfd1l in fatigue-affected tissues. Molecular docking indicated strong binding affinities between AKAP10, MTHFD1L, and repurposed drugs like irinotecan and digoxin. PheWAS revealed no significant pleiotropic effects for these genes.

Conclusions:

  • Mitochondria-related genes AKAP10 and MTHFD1L are strongly implicated as causal factors in chronic fatigue.
  • These genes represent promising therapeutic targets for chronic fatigue.
  • Repurposing existing drugs that interact with AKAP10 and MTHFD1L may offer novel treatment strategies, warranting further validation.