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Related Experiment Video

Updated: Mar 10, 2026

Morphological and Functional Evaluation of Axons and their Synapses during Axon Death in Drosophila melanogaster
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FUNDC1-dependent mitophagy determines axon regeneration capacity.

Wenlei Li1, Yujiao Liu1, Ruixuan Liu2

  • 1State Key Laboratory of Medicinal Chemical Biology and Frontier of Science Center for Cell Response, College of Life Sciences, Nankai University, Tianjin, China.

Autophagy
|March 8, 2026
PubMed
Summary

FUNDC1-mediated mitophagy is crucial for nerve regeneration by clearing damaged mitochondria. This process enhances axonal regrowth and peripheral nerve recovery through improved mitochondrial quality and carnosine biosynthesis.

Keywords:
Axon regenerationFUNDC1NRF1carnosinemitochondrial qualitymitophagy

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Mitochondrial Biology

Background:

  • Axon regeneration after nerve injury is essential for functional recovery.
  • Mitochondrial dysfunction can impede neuronal repair.
  • Mitophagy, the selective degradation of mitochondria, is a key cellular quality control process.

Purpose of the Study:

  • To investigate the role of FUN14 domain containing 1 (FUNDC1)-mediated mitophagy in neuronal axon regeneration.
  • To elucidate the molecular mechanisms by which FUNDC1 influences nerve repair.
  • To explore therapeutic strategies targeting mitophagy for enhanced peripheral nerve recovery.

Main Methods:

  • Overexpression and knockout of FUNDC1 in neuronal models.
  • In vitro and in vivo studies of axonal regeneration after nerve injury.
  • Metabolic profiling and molecular analysis of signaling pathways.
  • Treatment with mitophagy inducers like urolithin A.

Main Results:

  • FUNDC1 overexpression significantly enhanced axonal regeneration in vitro and in vivo.
  • FUNDC1-mediated mitophagy maintained mitochondrial health and promoted axon regrowth.
  • Mice lacking FUNDC1 showed impaired nerve regeneration, which was rescued by WT FUNDC1.
  • Metabolic analysis revealed enhanced carnosine biosynthesis driven by FUNDC1-mediated mitophagy, contributing to nerve recovery.

Conclusions:

  • FUNDC1-mediated mitophagy is a critical determinant of intrinsic neuronal regenerative capacity.
  • Targeting FUNDC1 and mitophagy offers a promising therapeutic avenue for peripheral nerve injury.
  • The study links mitochondrial quality control, metabolic adaptation, and nerve regeneration via FUNDC1.