MOTS-c

Repeated Heat Stress Modulates the Levels of the Mitokines MOTS-C and FGF21 in Active Men during Calf Muscle Immobilization

Circulating levels of MOTS-c in patients with breast cancer treated with metformin

Acute endurance exercise stimulates circulating levels of mitochondrial-derived peptides in humans

Effect of aerobic and resistance exercise on the mitochondrial peptide MOTS-c in Hispanic and Non-Hispanic White breast cancer survivors

β-Amyloid and mitochondrial-derived peptide-c are additive predictors of adverse outcome to high-on-treatment platelet reactivity in type 2 diabetics with revascularized coronary artery disease

Impact of Radiation Therapy on Serum Humanin and MOTS-c Levels in Patients with Lung or Breast Cancer

The Mitochondrial-Derived Peptide MOTS-c May Refine Mortality and Cardiovascular Risk Prediction in Chronic Hemodialysis Patients: A Multicenter Cohort Study

MOTS-c in type 2 diabetes mellitus: From risk factors to cardiac complications and potential treatment

Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging

Role of MOTS-c in the regulation of bone metabolism

MOTS-c Functionally Prevents Metabolic Disorders

MOTS-c: A potential anti-pulmonary fibrosis factor derived by mitochondria

Exercise, Mitohormesis, and Mitochondrial ORF of the 12S rRNA Type-C (MOTS-c)

[Effects of exercise intervention on mitochondrial-derived peptide MOTS-c in the germ cells of obese men]

MOTS-c: A Mitochondrial-Encoded Regulator of the Nucleus

MOTS-c: A novel mitochondrial-derived peptide regulating muscle and fat metabolism

MOTS-c: A promising mitochondrial-derived peptide for therapeutic exploitation

Mitochondrial-Encoded Peptide MOTS-c, Diabetes, and Aging-Related Diseases

MOTS-c, the Most Recent Mitochondrial Derived Peptide in Human Aging and Age-Related Diseases

A mitochondrial-derived peptide MOTS-c contributes to the protective effect against brain injury associated with LPS-induced sepsis by strengthening the blood-brain barrier's ultrastructure

MOTS-c attenuates lung ischemia-reperfusion injury via MYH9-Dependent nuclear translocation and transcriptional activation of antioxidant genes

Circulating PGC-1α and MOTS-c Peptide as Potential Mitochondrial Biomarkers in Patients Undergoing Aortic Valve Replacement

Mitochondria-derived peptide MOTS-c and its role in OSA pathogenesis: a potential therapeutic target?

Mitochondrial-encoded peptide MOTS-c prevents pancreatic islet cell senescence to delay diabetes

MOTS-c Impact on Muscle Cell Differentiation and Metabolism Across Fiber Types

MOTS-c attenuates mitochondrial dysfunction induces pyroptosis and cartilage degradation in osteoarthritis via an Nrf2-Dependent Mechanism

MOTS-c Levels and Sarcopenia Risk in Chronic Peritoneal Dialysis Patients: A Pilot Study

MOTS-c-modified functional self-assembly peptide hydrogels enhance the activity of nucleus pulposus-derived mesenchymal stem cells of intervertebral disc degeneration

Mitochondria-derived peptide MOTS-c restores mitochondrial respiration in type 2 diabetic heart

MOTS-C levels ın ındividuals with and without obesity and ıts association with ınflammation, insulin resistance and endothelial dysfunction

The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance

MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis

The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress.

MOTS-c reduces myostatin and muscle atrophy signaling.

MOTS-c interacts synergistically with exercise intervention to regulate PGC-1α expression, attenuate insulin resistance and enhance glucose metabolism in mice via AMPK signaling pathway.

Plasma MOTS-c levels are associated with insulin sensitivity in lean but not in obese individuals.

Circulating MOTS-c levels are decreased in obese male children and adolescents and associated with insulin resistance.

A pro-diabetogenic mtDNA polymorphism in the mitochondrial-derived peptide, MOTS-c.

The mitochondrial signaling peptide MOTS-c improves myocardial performance during exercise training in rats.

Mitochondrial derived peptide MOTS-c prevents the development of heart failure under pressure overload conditions in mice.