Mitochondrial open reading frame of the 12S rRNA type-c (MOTS-c) primes adrenal cortex metabolism.

Investigates MOTS-c's effects on adrenal cortex metabolic priming.

Mitochondria-derived peptide MOTS-c alleviates hyperoxia-induced bronchopulmonary dysplasia in neonatal mice by activating Nrf2 pathway.

Demonstrates MOTS-c protects against lung injury through Nrf2 antioxidant pathway activation.

MOTS-c Protects Against Acetaminophen-induced Liver Injury through the MAPK Signaling Pathway.

Shows MOTS-c provides hepatoprotection against acetaminophen-induced liver damage via MAPK signaling.

Mitochondrial-derived peptides MOTS-c and humanin attenuate dexamethasone-induced atrophy in human skeletal muscle cells.

Demonstrates MOTS-c protects against corticosteroid-induced muscle wasting in human cells.

Aerobic exercise and MOTS-c attenuate diabetic myocardial fibrosis via inhibition of the THBS1/TGF-beta signaling pathway.

Shows MOTS-c reduces cardiac fibrosis in diabetic models by inhibiting the THBS1/TGF-beta pathway.

Therapeutic Effects of MOTS-c in the Valproic Acid-Induced Autism Model in Rats.

Explores MOTS-c as a therapeutic agent in an autism model with effects via BDNF pathways.

Reduced serum and skeletal muscle MOTS c levels in women with polycystic ovary syndrome are associated with mitochondrial dysfunction.

Identifies reduced MOTS-c levels in women with PCOS linked to mitochondrial dysfunction.

MOTS-c attenuates cardiac dysfunction following high altitude exposure by promoting mitophagy.

Demonstrates MOTS-c protects the heart from high-altitude dysfunction by enhancing mitophagy.

Exogenous MOTS-c mitigates myocardial ischemia-reperfusion injury in rat heart models.

Provides evidence that exogenous MOTS-c protects against heart ischemia-reperfusion injury.