Publications by authors named "Angelo Madruga"
Article Synopsis
- Mitochondrial dysfunction can lead to serious health issues like mitochondrial myopathy, but scientists aren't sure how muscles react to this problem.
- Researchers studied mice with mitochondrial myopathy and found that signals about the dysfunction come from within the mitochondria themselves.
- They discovered that specific mitochondrial proteins activated a response (called mt-ISR) that helps muscles grow and survive by fixing issues in protein production, showing that this response is important across different types of tissues.
Mitochondrial dysfunction causes devastating disorders, including mitochondrial myopathy. Here, we identified that diverse mitochondrial myopathy models elicit a protective mitochondrial integrated stress response (mt-ISR), mediated by OMA1-DELE1 signaling. The response was similar following disruptions in mtDNA maintenance, from knockout of , and mitochondrial protein unfolding, from disease-causing mutations in CHCHD10 (G58R and S59L).
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- Interstitial stromal cells are essential for muscle development and repair, with specific expression of Hoxa11 and Hoxd11 important for muscle patterning during embryonic stages.
- Hoxa11-CreERT2 lineage tracing shows these cells contribute to muscle fibers in adulthood, surpassing contributions from traditional satellite cells.
- Isolated Hoxa11-expressing interstitial cells cannot form myotubes on their own, but can assist in the differentiation of myotubes, indicating they act as muscle progenitors rather than stem cells.