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MOTS-C
MOTS-C

MOTS-C

MOTS-C is a 16-amino-acid mitochondrial-derived peptide encoded within the mitochondrial 12S rRNA gene. It is studied for its role in mitochondrial–nuclear communication, particularly how cellular energy status may influence gene expression in preclinical systems.

Mechanistic Notes
AMPK Pathway Engagement
Preclinical studies indicate that MOTS-C:

  • Activates AMPK through modulation of the folate–AICAR cycle
  • Influences cellular energy-stress responses in vitro and in vivo animal models

Nucleus Translocation
Under metabolic stress, MOTS-C has been shown in research models to:

  • Translocate to the nucleus
  • Regulate gene expression via NRF2-associated pathways

Tissue Distribution
Research indicates a strong signal in:

  • Skeletal muscle
  • Liver
  • Adipose tissue

Metabolic Flexibility Models
Laboratory studies use MOTS-C to examine:

  • Mitochondrial signaling
  • Energy-homeostasis pathways
  • Stress-response adaptations


Clinical References

  1. Cell Metabolism (2015) — Energy-stress & metabolic-signaling mechanisms
  2. Cell Metabolism (2018) — Nuclear translocation & gene-regulation models
  3. Nature Communications (2021) — Exercise-response & muscle-homeostasis research
  4. Journal of Translational Medicine (2023) — Mechanistic mitochondrial-signaling review
  5. PMC Review (2022) — Age-related mitochondrial processes

*These findings are not clinical claims and not applicable to humans. They summarize animal and cell-based research.

Glucose & Metabolic Signaling

  • Increased glucose-infusion rates in metabolic-stress studies
  • Exercise-mimetic signaling patterns in skeletal muscle models

Cardiac & Mitochondrial Function

  • Improved mitochondrial efficiency and stress adaptation
  • Enhanced contractile function in cardiac-specific laboratory systems

Performance & Longevity Models

  • Increased maximal performance and lifespan in select preclinical organisms

Energy Expenditure & Obesity Models

  • Modulation of energy output and substrate utilization
  • Upregulation of thermogenic genes in adipose-tissue models

Bone & Mineral Studies

  • Maintenance of bone mass and mineral density in animal systems

Immune & Inflammatory Pathways

  • Downregulation of pro-inflammatory cytokines
  • Increased IL-10 in inflammation-response models
  • Regulatory T-cell modulation in autoimmune-study designs

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