Hormonal
Acute exercise induces mitophagy in skeletal muscle via an AMPK-dependent phosphorylation of Ulk1 at Serine 555, which is required for targeting damaged mitochondria to lysosomes.
Regular exercise triggers a specific cellular cleanup process (mitophagy) that removes damaged mitochondria. This process is driven by the AMPK-Ulk1 signaling pathway. To ensure this cleanup happens, consistent aerobic exercise is required to activate AMPK, which then phosphorylates Ulk1 to target damaged organelles for degradation.
These findings provide direct evidence of exercise-induced mitophagy and demonstrate the importance of Ampk-Ulk1 signaling in skeletal muscle.
Why this rating
High-quality mechanistic evidence using transgenic mouse models (dominant-negative and constitutively active AMPK, Ulk1 knockout) with direct visualization of mitophagy.
Source
Ampk phosphorylation of Ulk1 is required for targeting of mitochondria to lysosomes in exercise-induced mitophagy
Rhianna C. Laker et al. · Nature Communications · 2017
DOI 10.1038/s41467-017-00520-9
More from this paper
- AMPK is required for exercise-induced mitophagy, as blocking AMPK activity abolishes the increase in mitophagic markers (pure red puncta) following exercise.Good
- Ulk1 is required for the targeting of mitochondria to lysosomes during exercise-induced mitophagy, but is not required for lysosomal biogenesis itself.Good
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