MOTS-c news and clinical trials

A study found that MOTS-c protects against diabetic kidney injury in mice by downregulating LARS1, which promotes lipophagy and reduces tubular senescence and lipid deposition.

Laboratory experiments using aged mouse eggs and human granulosa cells showed that MOTS-c boosted energy production and supported egg maturation, though further research is needed for human fertility applications.

A study published in the Chinese Medical Journal found that MOTS-c mediates protection against lung ischemia-reperfusion injury through NRF2-dependent mitochondrial biogenesis.

Scientific Reports published a correction regarding a study linking reduced MOTS-c levels in women with polycystic ovary syndrome to mitochondrial dysfunction.

This review article discusses the potential of MOTS-c as a therapeutic candidate for sepsis-induced cardiomyopathy, noting that its translational relevance requires further disease-specific validation.

Researchers identified MOTS-c as a mitochondrial-encoded host defense peptide with antibacterial and immunomodulatory functions. It neutralized MRSA infectivity in a mouse model of acute peritonitis and reprogrammed human monocytes into macrophages with enhanced bacterial clearance.

The University of Gaziantep registered a prospective controlled study comparing the effects of general anesthesia and combined spinal-epidural anesthesia on ferroptosis, humanin, and MOTS-c levels in 68 renal transplant recipients.

Researchers testing MOTS-c on mesenchymal stromal cells from obese donors found that while the peptide activated AMPK signaling, it failed to improve renal perfusion in a mouse model of renal artery stenosis. Treatment also paradoxically increased senescence and inflammation in these cells.

Investigators found that MOTS-c treatment reduced fasting blood glucose and inflammatory markers in a high-fat diet and streptozotocin-induced diabetic rat model. Administration decreased levels of NLRP3 and other inflammasome components in left ventricular heart tissue.

A cross-sectional study found that circulating MOTS-c levels are significantly lower in patients with Hashimoto's thyroiditis compared to healthy controls. These reduced levels were independently associated with insulin resistance and autoimmune markers.

Researchers published a study showing that MOTS-c treatment in mice with C26 cancer cachexia significantly preserved skeletal muscle mass. The peptide reduced catabolic signaling and partially restored PGC-1α protein levels.

Researchers reviewed evidence showing that circulating MOTS-c levels are reduced in acute and chronic respiratory diseases. The findings suggest MOTS-c acts as a mitokine that modulates inflammation and oxidative stress, positioning it as a potential therapeutic candidate for lung diseases.

Investigators administered 53 µM of MOTS-c to isolated rat hearts subjected to ischemia-reperfusion injury. The treatment improved post-ischemic mechanical recovery, attenuated oxidative stress, and preserved mitochondrial functional integrity.

Researchers observed that Humanin and MOTS-c levels are downregulated in human atrial fibrillation tissue. Administering these peptides to mice reduced atrial fibrosis and mitochondrial dysfunction while lowering atrial fibrillation inducibility.

Researchers found that MOTS-c treatment improves survival of ischemic flaps by inhibiting PLA2G4A, which reduces lysosomal membrane permeability and enhances autophagy.

Scientists engineered R13A-MOTS-c for improved cellular uptake via LAT1-mediated transport to treat radiation-induced lung injury. Daily intraperitoneal administration of 5 mg/kg for 2 weeks mitigated pulmonary inflammation and oxidative stress in mice by activating the Nrf2 pathway.

Researchers studied 32 patients with peritoneal dialysis and found that higher urinary MOTS-c levels correlated with lower systemic oxidative stress, while higher peritoneal levels were associated with an improved vascular profile.

Researchers showed that MOTS-c attenuates hyperoxia-induced cardiac injury in neonatal mice by inhibiting oxeiptosis. The peptide interacts with KEAP1 to maintain the KEAP1-PGAM5 interaction and prevent downstream AIFM1 nuclear translocation.

New paper in Biomedicines: The Association Between Serum MOTS-c Levels and Myocardial Ischemia-Reperfusion Injury in Patients with Acute Myocardial Infarction: A Cross-Sectional Study.

The FDA announced a public advisory committee meeting of the Pharmacy Compounding Advisory Committee to seek input on bulk drug substances nominated for the Section 503A bulk drug substances list.

Researchers investigating MOTS-c levels in adolescents with polycystic ovary syndrome (PCOS) found no significant difference compared to healthy controls. The study also observed no significant association between the m.1382A>C gene polymorphism and PCOS.

Researchers found that MOTS-c preserves spermatogenesis by targeting SLC7A11 to suppress ferroptosis and oxidative stress. Exogenous administration ameliorated spermatogenic impairment induced by mechanical stress in mice.

Hudson Biotech registered a Phase 2 trial of MOTS-c to evaluate if 12 weeks of treatment improves insulin sensitivity in 120 adults with prediabetes and overweight or obesity.

Researchers analyzed the effects of MOTS-c on rat adrenal tissue. The peptide modulated lipid metabolism and upregulated calcium signaling, but it did not directly drive steroidogenesis or alter basal hormone levels.

A study in neonatal mice found that MOTS-c alleviates hyperoxia-induced bronchopulmonary dysplasia by activating the Nrf2 pathway. The peptide reduced lung alveolar simplification and improved angiogenesis.

Researchers tested MOTS-c in a mouse model of acetaminophen-induced liver injury. MOTS-c treatment reduced liver damage, inflammation, and oxidative stress by suppressing components of the MAPK signaling pathway.

Researchers tested whether the mitochondrial-derived peptides MOTS-c and S14G-humanin could mitigate muscle atrophy in human myotubes induced by 10 µM dexamethasone. Co-treatment with MOTS-c preserved myotube area and fusion index, while HNG co-treatment also preserved myotube area.

Researchers examined the effects of aerobic exercise and MOTS-c on diabetic myocardial fibrosis. Both approaches improved metabolism and reduced collagen buildup by inhibiting the THBS1/TGF-β signaling pathway.

Researchers studied MOTS-c in a rat model of autism induced by valproic acid. They found MOTS-c reversed most autism-like behaviors and neuronal damage, but did not significantly change plasma BH4 or BDNF levels.

Researchers compared serum and skeletal muscle MOTS-c levels in 40 women with PCOS against 40 controls. Women with PCOS had significantly lower circulating MOTS-c (220.2 ± 147.6 pg/mL) and reduced skeletal muscle expression.

A study in mice demonstrated that exogenous MOTS-c supplementation alleviates cardiac dysfunction induced by high altitude exposure. The peptide promotes mitophagy through the Pink1/Parkin pathway, helping to maintain mitochondrial quality.

Researchers identified 0.5 mg/kg as the optimal dose of exogenous MOTS-c to protect isolated rat hearts from ischemia-reperfusion injury in an ex vivo study. This dose produced a 73% reduction in infarct size and improved heart function.

Researchers compared MOTS-c levels in lean controls and obese patients. Obese participants showed higher MOTS-c (273 ± 56 vs. 223 ± 50 pg/mL), and these levels remained unchanged six months after bariatric surgery.