Carlos Henríquez‐Olguín

Site-resolved redox proteomics of human muscle after three exercise types shows modality-specific cysteine oxidation, and a p62 Cys113 switch tied to autophagy in myotubes and mitochondrial remodeling in mice.

This study develops bioengineered human skeletal muscle tissues that mature metabolically and functionally, capturing key aspects of glucose metabolism and response to exercise and pharmacological agents.

This study shows that blocking ActRIIA/IIB increases muscle mass and strength in mice but causes glucose intolerance and reduced voluntary activity.

This study uses chemogenetics to induce mitochondrial H2O2 in skeletal muscle and shows it causes dose-dependent atrophy without structural damage.

This study identifies SLIRP as a mitochondrial mRNA stabilizing protein that regulates mitochondrial structure and respiration in skeletal muscle, with exercise improving mitochondrial function through increased mitoribosome capacity.

This study identifies Rac1 as a key regulator of exercise training adaptations by showing its role in protein synthesis, glycogen resynthesis, and running capacity in mice and human muscle.

This study shows that AMPK is upregulated in human cachectic muscle and that AMPK deficiency in mice worsens cancer-induced metabolic dysfunction and cachexia.

This study reveals that RNA-bound PGC-1α forms liquid-like nuclear condensates to regulate gene expression and transcriptional networks in response to metabolic stimuli.