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Molecular Formula | C₁₀₁H₁₅₂N₂₈O₂₂S₂ |
CAS Number | 1627580-64-6 |
Molar Mass | 2174.60 g/mol |
Amino Acid Sequence | Met-Arg-Trp-Gln-Glu-Met-Gly-Tyr-Ile-Phe-Tyr-Pro-Arg-Lys-Leu-Arg |
PubChem CID | 146675088 |
Primary Research Area |
Metabolic Actions Skeletal Muscle Glucose Metabolism Obesity & Diabetes Regulation Exercise & Longevity Insulin Resistance Stress Adaptation Anti-inflammatory Processes Neuroprotection Aging-Related Pathologies Brown Adipose Tissue (BAT) Activation |
Purity | >99% |
Research Summary | Description |
---|---|
The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces insulin resistance |
Summary: This study highlighted MOTS-C's significant role in glucose metabolism. It targets skeletal muscle to enhance glucose uptake and has implications for obesity, diabetes, exercise, and longevity. Citation: Lee, C., Zeng, J., Drew, B. G., Sallam, T., Martin-Montalvo, A., Wan, J.,... & Cohen, P. (2015). The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces insulin resistance. Cell Metabolism, 21(1), 113-124. |
A cell-penetrating MOTS-c analogue enhances memory and attenuates neuroinflammation in the hippocampus |
Summary: Investigations have shown MOTS-C exhibiting anti-inflammatory effects by modulating key molecules like AMPK, SIRT1, and NF-κB, and by inhibiting reactive oxygen species (ROS) production. Furthermore, a cell-penetrating MOTS-C analogue has been shown to enhance memory and attenuate neuroinflammation in the hippocampus. Citation: Jiang, L., Li, Y., Li, X., Wang, Y., & Zhang, Y. (2021). A cell-penetrating MOTS-c analogue enhances memory and attenuates neuroinflammation in the hippocampus. Journal of Neuroinflammation, 18(1), 1-15. |
MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis |
Summary: This study investigated the role of MOTS-c in physical performance and aging. It demonstrated that MOTS-c levels in both human skeletal muscle and circulation are increased by exercise. In mice, exogenous administration of MOTS-c improved exercise capacity, grip strength, and protected against age-dependent physical decline. It also influenced muscle metabolism and gene expression, promoting a more youthful metabolic profile in aged muscles. These effects were linked to its role in regulating metabolic pathways crucial for muscle function and resilience. Citation: Reynolds, J. C., Jo, Y. S., Palmer, C. S., Lee, C., & Cohen, P. (2021). MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis. Nature Communications, 12(1), 470. https://doi.10388/s41467-020-20790-0 |
MOTS-c reduces myostatin and muscle atrophy signaling |
Summary: This study explored the relationship between MOTS-c and myostatin, a well-known negative regulator of muscle growth. The researchers found an inverse correlation between plasma MOTS-c and myostatin levels in humans. In animal models, MOTS-c treatment was shown to reduce myostatin expression and activity, as well as downstream signaling pathways associated with muscle atrophy (e.g., SMAD2/3 phosphorylation and atrogene expression). This suggests a mechanism by which MOTS-c could counteract muscle wasting. Citation: Fuku, M., Ohno, R., Kono, J., Kim, K. H., Cohen, P., & Ishii, M. (2021). MOTS-c reduces myostatin and muscle atrophy signaling. FASEB Journal, 35(6), e21550. https://doi.org/10.1096/fj.202002570R |
Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging |
Summary: MOTS-C is recognized for its role in maintaining energy and stress homeostasis, thereby promoting healthy aging. Its expression decreases with aging, suggesting that its decline may contribute to age-related physiological changes. Citation: Reynolds, J. C., Lee, C., & Cohen, P. (2021). Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging. Aging Cell, 20(1), e13292. |
"Mitochondrial-encoded peptide MOTS-c, diabetes, and aging-related diseases " |
Summary: This review article summarizes the therapeutic potential of MOTS-c in diabetes and age-related diseases. It highlights MOTS-c's ability to regulate T-cell differentiation and activation (e.g., upregulation of Treg cells) in an mTORC1-dependent manner. This immunoregulatory function was shown to prevent pancreatic infiltration of autoreactive T-cells in non-obese diabetic (NOD) mice, a model for type 1 diabetes. MOTS-c also improved glucose tolerance and insulin secretion and protected pancreatic beta-cells. The review further discusses MOTS-c's broader impact on metabolic adaptability and age-related conditions. Citation: Kim, H., & Lee, J. Y. (2023). Mitochondrial-Encoded Peptide MOTS-c, Diabetes, and Aging-Related Diseases. Diabetes & Metabolism Journal, 47(2), 143–153. https://doi.org/10.4093/dmj.2022.0360 |
Summary: This study highlighted MOTS-C's significant role in glucose metabolism. It targets skeletal muscle to enhance glucose uptake and has implications for obesity, diabetes, exercise, and longevity.
Citation: Lee, C., Zeng, J., Drew, B. G., Sallam, T., Martin-Montalvo, A., Wan, J.,... & Cohen, P. (2015). The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces insulin resistance. Cell Metabolism, 21(1), 113-124.
Summary: Investigations have shown MOTS-C exhibiting anti-inflammatory effects by modulating key molecules like AMPK, SIRT1, and NF-κB, and by inhibiting reactive oxygen species (ROS) production. Furthermore, a cell-penetrating MOTS-C analogue has been shown to enhance memory and attenuate neuroinflammation in the hippocampus.
Citation: Jiang, L., Li, Y., Li, X., Wang, Y., & Zhang, Y. (2021). A cell-penetrating MOTS-c analogue enhances memory and attenuates neuroinflammation in the hippocampus. Journal of Neuroinflammation, 18(1), 1-15.
Summary: This study investigated the role of MOTS-c in physical performance and aging. It demonstrated that MOTS-c levels in both human skeletal muscle and circulation are increased by exercise. In mice, exogenous administration of MOTS-c improved exercise capacity, grip strength, and protected against age-dependent physical decline. It also influenced muscle metabolism and gene expression, promoting a more youthful metabolic profile in aged muscles. These effects were linked to its role in regulating metabolic pathways crucial for muscle function and resilience.
Citation:
Reynolds, J. C., Jo, Y. S., Palmer, C. S., Lee, C., & Cohen, P. (2021). MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis. Nature Communications, 12(1), 470. https://doi.10388/s41467-020-20790-0
Summary: This study explored the relationship between MOTS-c and myostatin, a well-known negative regulator of muscle growth. The researchers found an inverse correlation between plasma MOTS-c and myostatin levels in humans. In animal models, MOTS-c treatment was shown to reduce myostatin expression and activity, as well as downstream signaling pathways associated with muscle atrophy (e.g., SMAD2/3 phosphorylation and atrogene expression). This suggests a mechanism by which MOTS-c could counteract muscle wasting.
Citation:
Fuku, M., Ohno, R., Kono, J., Kim, K. H., Cohen, P., & Ishii, M. (2021). MOTS-c reduces myostatin and muscle atrophy signaling. FASEB Journal, 35(6), e21550. https://doi.org/10.1096/fj.202002570R
Summary: MOTS-C is recognized for its role in maintaining energy and stress homeostasis, thereby promoting healthy aging. Its expression decreases with aging, suggesting that its decline may contribute to age-related physiological changes.
Citation: Reynolds, J. C., Lee, C., & Cohen, P. (2021). Mitochondria-derived peptide MOTS-c: effects and mechanisms related to stress, metabolism and aging. Aging Cell, 20(1), e13292.
Summary: This review article summarizes the therapeutic potential of MOTS-c in diabetes and age-related diseases. It highlights MOTS-c's ability to regulate T-cell differentiation and activation (e.g., upregulation of Treg cells) in an mTORC1-dependent manner. This immunoregulatory function was shown to prevent pancreatic infiltration of autoreactive T-cells in non-obese diabetic (NOD) mice, a model for type 1 diabetes. MOTS-c also improved glucose tolerance and insulin secretion and protected pancreatic beta-cells. The review further discusses MOTS-c's broader impact on metabolic adaptability and age-related conditions.
Citation:
Kim, H., & Lee, J. Y. (2023). Mitochondrial-Encoded Peptide MOTS-c, Diabetes, and Aging-Related Diseases. Diabetes & Metabolism Journal, 47(2), 143–153. https://doi.org/10.4093/dmj.2022.0360
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