Dossier overview
4
research areas
3
references
3
handling notes
01
Mechanism of action
Research literature has associated MOTS-c with AMPK pathway activation, nuclear translocation under metabolic stress (NRF2-related antioxidant gene regulation), and modulation of myostatin / muscle atrophy signalling in cell and mouse models.
02
Research applications
- Mitochondrial-derived peptide biology
- Metabolic homeostasis and insulin resistance research
- Skeletal muscle atrophy research
- AMPK and NRF2 pathway research
Evidence at a glance
What's behind this profile
3 citations · 2015–2021
- Animal
- 3
Studies in rodents or other animal models.
Publication years
- 15
- 16
- 17
- 18
- 19
- 20
- 21
Counts are derived from the cited studies below. A study covering both in vivo and in vitro work is counted by its primary model. Sample size is reported in 0 of 3 citations. Findings remain model-specific and are not extrapolated to therapeutic use.
03
Study references
Each profile cites a minimum of two peer-reviewed sources, with model type and reported sample size where the source provides it. Findings are model-specific and must not be extrapolated to therapeutic use.
The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance
2015
Lee C et al. · Cell Metabolism
- Model
- In vivo and in vitro — mouse models of diet-induced obesity and skeletal muscle assays
- Sample
- Not reported in abstract
Reported that MOTS-c prevented diet-induced obesity and insulin resistance and activated AMPK in skeletal muscle in the mouse models used.
The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress
2018
Kim KH et al. · Cell Metabolism
- Model
- In vitro mechanistic cellular studies with in vivo mouse correlates
- Sample
- Not reported in abstract
Reported MOTS-c nuclear translocation under metabolic stress and AMPK-dependent regulation of antioxidant via NRF2 interaction.
MOTS-c reduces myostatin and muscle atrophy signaling
2021
Kumagai H et al. · American Journal of Physiology — Endocrinology and Metabolism
- Model
- In vitro skeletal muscle cell models and in vivo mouse correlates
- Sample
- Not reported in abstract
MOTS-c was associated with reduced myostatin expression and muscle atrophy signalling via the CK2-PTEN-mTORC2-AKT-FOXO1 pathway in the models used.
Evidence caveats
- All cited primary studies are preclinical (mouse and cell models). No PubMed-indexed controlled human clinical trials are cited on this profile.
- MOTS-c is a relatively recently discovered peptide (2015); independent replication across research groups is still accumulating.
04
Storage and handling
Store under controlled laboratory conditions with batch and preparation details recorded.
- Maintain batch and supplier documentation for short-peptide comparison work.
- Protect material from contamination during handling.
- Use protocol-specific storage documentation.