Reynolds. Joseph C JC; Lai. Rochelle W RW; Woodhead. Jonathan S T JST; Joly. James H JH; Mitchell. C...
A tiny protein made by mitochondria called MOTS‑c can boost muscle performance and slow age‑related decline in mice, and regular exercise raises its levels in people. Giving mice the peptide a few times a week, even when they’re old, helped them stay stronger and healthier for longer.
Lu. Huanyu H; Wei. Ming M; Zhai. Yue Y; Li. Qingyang Q; Ye. Zichen Z; Wang. Li L; Luo. Wenjing W; Ch...
In mice that had their ovaries removed (a model for menopause), giving the tiny mitochondrial peptide MOTS‑c stopped weight gain, kept blood sugar normal, and helped fat tissue stay healthy. It did this by turning on brown fat and the AMPK energy‑regulating pathway, which together boost calorie burning and reduce inflammation.
Kołodziejski. Paweł A PA; Pruszyńska-Oszmałek. Ewa E; Wojciechowicz. Tatiana...
The paper reviews new peptide hormones, including MOTS‑c, that affect how fat cells grow and work. It shows that these molecules can influence both white fat (energy storage) and brown fat (energy burning) in lab and animal studies, suggesting they might help with weight and metabolic health.
Kim. Kyung Hwa KH; Son. Jyung Mean JM; Benayoun. Bérénice A BA; Lee. Changhan C
MOTS‑c is a tiny protein made by mitochondria that can move into the cell nucleus when you’re low on glucose or under other metabolic stress. Once there, it helps turn on a bunch of genes that protect cells from damage, working together with the AMPK energy sensor and the NRF2 stress‑response system. This shows that mitochondria can directly tell the nucleus what to do, adding a new layer to how cells adapt to stress.
Yang. Boyu B; Yu. Qiongli Q; Chang. Bo B; Guo. Qi Q; Xu. Sitong S; Yi. Xuejie X; Cao. Shicheng S
In mice, the mitochondrial peptide MOTS‑c works together with exercise to boost a muscle‑building factor (PGC‑1α), turn on AMPK, and improve insulin sensitivity and glucose handling. When mice were given MOTS‑c or made to run, their muscle and blood levels of the peptide rose, and they showed better metabolic markers, especially compared to obese mice on a high‑fat diet.
In mice, regular running raises the amount of the mitochondrial peptide MOTS‑c in leg muscles, and this boost sticks around even after a few weeks without exercise. Giving an untrained mouse a single dose of MOTS‑c makes it run longer and farther in a short‑term test. The peptide also moves into the nucleus of certain muscles after a downhill run, hinting at a signaling role.
MOTS‑c is a tiny protein made by mitochondria that gets released when you’re stressed or exercising. It moves into the cell nucleus and turns on genes that help the body handle stress, improve energy use, and protect against age‑related problems. Most of its effects come from activating a pathway (Folate‑AICAR‑AMPK) that boosts metabolism, reduces insulin resistance, and calms inflammation.
In rats, giving the mitochondrial peptide MOTS‑c or doing regular aerobic exercise both made the heart bigger, the muscle fibers thicker, and improved how well the heart pumped, without raising harmful pressure. These benefits were linked to activation of a specific signaling pathway (NRG1‑ErbB4‑C/EBPβ). The peptide acted in a very similar way to exercise.
Yan. Zhao Z; Zhu. Shu S; Wang. Hanli H; Wang. Li L; Du. Tianshu T; Ye. Zichen Z; Zhai. Dongsheng D;...
A tiny protein called MOTS‑c, which is made in mitochondria, was given to mice that had bone loss caused by wear‑particle inflammation (like what can happen around joint implants). The peptide reduced bone erosion and inflammation by making bone‑forming cells release more of a protective factor (OPG) and less of a bone‑resorbing signal (RANKL), and by dampening inflammatory pathways (NF‑κB and STAT1) through an AMPK‑PGC‑1α‑ROS mechanism.
Ikonomidis. Ignatios I; Katogiannis. Konstantinos K; Kyriakou. Elias E; Taichert. Maria M; Katsimagl...
In people with type‑2 diabetes and heart disease, having overly sticky platelets (high on‑clopidogrel platelet reactivity) together with either high blood beta‑amyloid or low levels of the mitochondrial peptide MOTS‑c sharply raises the chance of a heart attack or death over two years. The study shows these three factors add up to predict risk, and the finding was confirmed in another group of patients.
The study shows that during severe inflammation (like sepsis), a protein called DNA‑PKcs shuts down the production of the mitochondrial peptide MOTS‑c, which then leads to damage in tiny heart blood vessels. Blocking DNA‑PKcs or giving extra MOTS‑c protects those vessels by keeping a stress‑signal pathway (JNK) turned off and preserving the cell’s internal scaffolding.
MOTS‑c is a tiny peptide made by mitochondria that acts like a hormone. It can improve insulin sensitivity, help prevent weight gain, boost muscle and bone health, support the immune system, and may slow aging. It does this mainly by turning on the AMPK energy‑sensing pathway and tweaking the folate‑methionine cycle, which in turn changes genes such as GLUT4, STAT3 and IL‑10.
Qin. Qing Q; Delrio. Silvia S; Wan. Junxiang J; Jay Widmer. R R; Cohen. Pinchas P; Lerman. Lilach O...
People with bad coronary blood vessel function have lower levels of the mitochondrial peptide MOTS‑c in their blood, and in lab tests MOTS‑c helped rat and mouse vessels respond better to signals that make them relax. This suggests that MOTS‑c might be important for keeping blood vessels healthy, but we don’t yet know how to safely boost it in humans.
MOTS‑c is a tiny protein made by mitochondria that helps the body make more AICAR, a natural compound that turns on the AMPK pathway, which is known to improve metabolism. In animal studies it reduced obesity and insulin resistance, hinting it could help prevent type‑2 diabetes and slow aging, but human data and dosing guidelines are still missing.
Wei. Ming M; Gan. Lu L; Liu. Zheng Z; Liu. Li L; Chang. Jin-Rui JR; Yin. Da-Chuan DC; Cao. Hui-Ling...
In rats, daily injections of the tiny mitochondrial peptide MOTS‑c (5 mg per kg body weight) for four weeks reduced the hardening of blood vessels caused by excess vitamin D3 and nicotine. The peptide boosted a protective protein called AMPK and lowered two receptors (AT‑1 and ET‑B) that normally promote blood‑vessel damage.
Yaşar. E E; Çakmak. T T; Bayramoğlu. A A; Karakuş. Y Y; Tekin. S S; Şek...
People with stable heart disease have lower blood levels of a tiny protein called MOTS‑c, and those levels can predict how severe the artery blockages are. The study suggests MOTS‑c could be used as a blood test to spot hidden heart problems early, but it doesn’t tell us how to raise it or whether taking it helps.
Exercise can raise the level of a tiny protein called MOTS‑c in the sperm‑producing cells of overweight men, and higher MOTS‑c is linked to better sugar handling and less fat. This suggests that regular workouts might help improve metabolic health and male fertility in obese individuals.
Wu. Jiaqi J; Xiao. Danrui D; Yu. Kaiwen K; Shalamu. Kudureti K; He. Ben B; Zhang. Min M
A study found that the mitochondrial peptide MOTS‑c can protect heart cells from damage caused by severe bacterial infection (sepsis) in lab experiments. It lowers inflammation, reduces oxidative stress, and prevents cell death by turning on the AMPK pathway. Blocking AMPK removes these benefits, showing the pathway is essential for MOTS‑c’s effect.
Dieli-Conwright. Christina M CM; Sami. Nathalie N; Norris. Mary K MK; Wan. Junxiang J; Kumagai. Hiro...
A 16‑week program of combined aerobic and resistance training raised the blood level of the mitochondrial peptide MOTS‑c in non‑Hispanic White women who had survived breast cancer. The rise was linked to losing fat, gaining lean muscle, and better insulin and inflammation markers. Hispanic participants did not show the same peptide increase.
Scientists discovered that the tiny protein MOTS‑c, which is made inside mitochondria, can move into the cell nucleus when the cell is stressed and directly turn genes on or off. This shows that mitochondria can send signals to the nucleus, not just the other way around.