MOTs-C 40 mg

▎ MOTs-C Structure

▎ MOTs-C Kev Tshawb Fawb

Kev tshawb fawb keeb kwm ntawm MOTs-C yog dab tsi?

Mitochondria, ua haujlwm raws li 'powerhouse' ntawm cov hlwb, ua lub luag haujlwm tseem ceeb hauv kev tswj hwm cellular homeostasis. Cov txheej txheem kev sib txuas lus ntawm mitochondria thiab cov nucleus tau ntev tau ua kom pom tseeb ntawm kev tshawb fawb. Mitochondria muaj kev ywj pheej genome. Tshaj li ntawm 37 cov noob caj noob ces, cov kev tshawb fawb tsis ntev los no tau qhia tias mitochondrial DNA kuj encodes biologically nquag nquag peptides, ib qho ntawm cov mitochondrial-derived peptide MOTs-C, encoded los ntawm mitochondrial 12S rRNA cheeb tsam. Qhov kev tshawb pom no nthuav dav dav ntawm cov noob caj noob ces mitochondrial, muab cov kev xav tshiab rau kev nthuav tawm cov txheej txheem lom neeg tseem ceeb xws li mitochondrial-nuclear kev sib txuas lus thiab kev tswj hwm metabolic.

Tam sim no, kev kho mob rau ntau yam kab mob nyuaj xws li cov metabolism thiab kab mob siab B mob ntev yuav ntsib teeb meem tseem ceeb. MOTs-C lub luag haujlwm tseem ceeb hauv kev tswj cov leeg nqaij pob txha metabolic, xws li kev txhim kho cov piam thaj metabolism, qhia nws lub peev xwm los kho cov kab mob metabolic. Tsis tas li ntawd, qhov txawv txav MOTs-C qib tau pom nyob rau hauv ntau yam txheej txheem kab mob tau ua rau cov kws tshawb fawb los tshawb xyuas nws lub luag haujlwm hauv kab mob pib, kev loj hlob, thiab kev kho mob, nrhiav txoj hauv kev tshiab los daws cov teeb meem tsis zoo no.

Yuav ua li cas yog lub mechanism ntawm kev txiav txim rau MOTs-C?

Regulating Diabetes-Related Signaling Pathways

Ua kom AICAR-AMPK Txoj Kev Qhia Tawm: MOTs-C qhib txoj hauv kev AICAR-AMPK los ntawm kev cuam tshuam lub voj voog intracellular folate-methionine. Activated AMPK tswj cov cellular zog metabolism, xws li txhawb cov piam thaj uptake thiab fatty acid oxidation. Hauv cov metabolism hauv qabzib, nws nce qhov kev hloov pauv ntawm cov piam thaj thauj mus rau GLUT4 mus rau cov cell membrane, yog li txhim kho cov piam thaj hauv cellular, txhim kho insulin tsis kam, thiab pab tiv thaiv thiab kho cov kab mob metabolic zoo li hom 2 metabolism ^[1].

Qhov cuam tshuam rau Lwm Txoj Kev: Tshaj li AMPK txoj hauv kev, MOTs-C kuj ua rau txoj hauv kev AKT, txoj kev oxidative kev nyuaj siab, thiab txoj kev mob ntsig txog. Hais txog AKT txoj hauv kev, nws tuaj yeem cuam tshuam cov txheej txheem ntawm tes xws li kev loj hlob, kev loj hlob, thiab kev ciaj sia los ntawm kev tswj hwm txoj kev ua haujlwm. Nyob rau hauv txoj kev oxidative kev nyuaj siab, MOTs-C txo cov theem ntawm oxidative kev nyuaj siab nyob rau hauv lub cellular, txo reactive oxygen hom (ROS) ntau lawm, thiab tiv thaiv hlwb los ntawm oxidative puas. Nyob rau hauv txoj kev o, nws suppresses tso tawm inflammatory mediators thiab alleviates inflammatory teb. Piv txwv li, nyob rau hauv inflammatory mob qauv, MOTs-C txo cov inflammatory mediator tso tawm nyob rau hauv lub dorsal horn ntawm tus txha caj qaum, yog li txhim kho cov tsos mob ntawm tus mob ^[2].

Daim duab 1 Cov haujlwm tseem ceeb ntawm MOTs-C suav nrog txo cov tshuaj insulin, tiv thaiv kev rog, txhim kho cov leeg nqaij, txhawb cov pob txha metabolism, txhim kho kev tiv thaiv kab mob, thiab ncua kev laus ^[1].

Kev cai ntawm Gene Expression

Nuclear Gene Expression Regulation: Thaum cov hlwb ntsib kev ntxhov siab hauv metabolic, xws li kev txwv cov piam thaj thiab oxidative kev nyuaj siab, MOTs-C hloov mus rau lub nucleus kom ncaj qha tswj cov kev hloov pauv ntawm cov noob caj noob ces, yog li txhawb kev ua haujlwm ntawm lub cev. Piv txwv li, MOTs-C modulates cov kev qhia ntawm cov metabolism hauv cov noob xws li GLUT4, STAT3, thiab IL-10, cuam tshuam cov txheej txheem physiological nrog rau cov piam thaj metabolism thiab kev tiv thaiv kab mob. Kev nthuav qhia GLUT4 nce ntxiv txhawb nqa cov piam thaj hauv cellular; STAT3 koom nrog hauv kev loj hlob ntawm tes, kev sib txawv, thiab kev tiv thaiv kab mob; IL-10, ib qho tshuaj tiv thaiv kab mob cytokine, txo cov lus teb inflammatory thaum nws qhia tau siab ^[1,3].

Txhawb Zog Ntshav Qab Zib

Enhanced Glycolysis: Hauv ntau hom kab mob, xws li lub ntsws ischemia-reperfusion raug mob (LIRI) qauv tshwm sim los ntawm cardiopulmonary bypass (CPB), MOTs-C pretreatment txhim kho glycolytic flux hauv pulmonary microvascular endothelial hlwb (PMVECs). Nws txo qis LIRI kev raug mob los ntawm kev kho cov cellular zog homeostasis thiab txo cov lipid peroxidation los ntawm kev txhim kho tus tseem ceeb glycolytic enzyme PFKFB3. Qhov no qhia tau hais tias MOTs-C modulates glycolytic txoj hauv kev los muab lub zog txaus rau cov hlwb hauv kev ntxhov siab, yog li tswj hwm cov cellular ua haujlwm ^[4].

Cellular Protection Effects

Mitigation of Mitochondrial Damage: Hauv cov qauv hluav taws xob pneumonitis (RP), MOTs-C txo qis cov nqaij mos raug mob, mob, thiab oxidative kev nyuaj siab thaum thim rov qab alveolar epithelial cell apoptosis thiab mitochondrial puas. Cov txheej txheem no suav nrog kev nce qib ntawm cov khoom siv hluav taws xob E2-txog qhov cuam tshuam 2 (Nrf2) qib thiab txhawb nqa nws txoj kev hloov pauv nuclear. Nrf2 ua kom muaj cov tshuaj tiv thaiv kab mob antioxidant thiab cell-tiv thaiv cov noob, tiv thaiv kev ua haujlwm mitochondrial. Qhov no qhia tau tias MOTs-C tiv thaiv cov ntaub so ntswg puas los ntawm kev khaws cia mitochondria thiab txo qis apoptosis ^[5].

Kev Tiv Thaiv Lwm Cov Cells: Hauv kev tshawb fawb ntawm Duchenne cov leeg nqaij dystrophy (DMD), MOTs-C tau pom tias muaj cov nqaij leeg-tshuaj. Nws txhim kho glycolytic flux thiab lub zog tsim muaj peev xwm hauv cov leeg dystrophic, pab txhawb kev txhim kho cov leeg nqaij. Tsis tas li ntawd, hauv cov qauv mob inflammatory, MOTs-C tswj hwm hauv nruab nrab lossis peripheral alleviates mob hypersensitivity los ntawm suppressing inflammatory teb thiab neuronal hyperexcitability, muab cov teebmeem neuroprotective ^[2,6].

Dab tsi yog cov ntawv thov ntawm MOTs-C?

Kev Kho Mob Metabolic Disorders:

Txhim kho insulin tsis kam thiab tiv thaiv cov metabolism: MOTs-C txhim kho cov tshuaj insulin, uas yog qhov tseem ceeb rau kev tiv thaiv hom 2 metabolism. Insulin tsis kam yog qhov tseem ceeb hauv qhov pib ntawm hom 2 metabolism. MOTs-C tuaj yeem txhim kho insulin rhiab heev los ntawm kev ua kom lub AICAR-AMPK taw qhia txoj hauv kev thiab tswj lub voj voog intracellular folate-methionine. Kev tshawb fawb los ntawm Gao Y qhia tias nws txhawb nqa cov leeg nqaij pob txha thiab kev siv, zoo li qhib txoj hauv kev ntxiv cov piam thaj hauv cov hlwb, yog li txo cov ntshav qabzib ntau ^[1].

Kev tswj cov lipid metabolism thiab tiv thaiv kev rog: Hais txog lipid metabolism, MOTs-C nce cov roj rog xim av thermogenesis thiab txhawb cov rog dawb. Cov roj xim av siv lub zog los ntawm thermogenesis, thaum cov roj dawb browning qhia txog kev hloov pauv ntawm lub zog khaws cia cov rog dawb rau hauv lub zog siv roj xim av. Cov txheej txheem no pab lub cev hloov mus rau qhov txias thiab, qhov tseem ceeb tshaj, tiv thaiv kev rog rog thiab lipid metabolism tsis zoo, muab cov kev xav tshiab rau kev tiv thaiv kev rog rog ^[1].

Kev Tiv Thaiv thiab Kev Kho Mob Ntawm Cov Mob Muscle-Related:

Txhawb nqa cov leeg sib txawv: Cov kev tshawb fawb hauv vitro qhia tias cov tsiaj qus-hom MOTs-C peptide txhim kho myotubular tsim hauv tib neeg (LHCN-M2) thiab nas (C2C12) cov leeg nqaij progenitor hlwb, thaum Y8F mutant peptide tsis muaj cov nyhuv no. Cov kev tshawb fawb ntxiv tau qhia tias MOTs-C txhim kho myotubulogenesis los ntawm kev cuam tshuam nrog IL-6 / Janus kinase / signal transducer thiab activator ntawm transcription 3 (STAT3) txoj hauv kev, yog li txo cov kev ua STAT3 transcriptional ^[7].

Tiv thaiv cov leeg nqaij Atrophy: Plasma MOTs-C qib tsis zoo cuam tshuam nrog cov qib myostatin. MOTs-C tiv thaiv palmitate-induced myotube atrophy nyob rau hauv sib txawv C2C12 hlwb thiab txo cov ntshav plasma myostatin nyob rau hauv cov zaub mov-vim cov nas rog rog. Nws tiv thaiv cov leeg nqaij atrophy los ntawm kev txhim kho AKT phosphorylation, inhibiting qhov kev ua ntawm FOXO1 - ib qho kev hloov pauv ntawm myostatin thiab lwm cov leeg nqaij atrophy - thaum tswj mTORC2 thiab PTEN kev ua ub no thiab nce CK2 kev ua ub no txhawm rau txhawm rau PTEN ^[8].

Los tiv thaiv kev laus: MOTs-C qhia kev hloov pauv tau txuas nrog kev laus, thiab nws nthuav tawm cov khoom tiv thaiv kev laus. Qhov no tau ua tiav los ntawm ntau lub tswv yim, suav nrog kev txhim kho cov piam thaj thiab lipid metabolism, txhim kho cellular mitochondrial muaj nuj nqi, thiab txo cov kab mob hauv lub cev. Kev tshawb fawb los ntawm Gao Y et al. qhia tau hais tias kev txhim kho cov metabolism muab cov hlwb nrog ntau dua thiab ruaj khov zog. Txhim kho mitochondrial muaj nuj nqi zoo ib yam li kev kho dua tshiab ntawm lub cell 'zog Hoobkas,' thaum txo cov inflammatory teb txo qis inflammatory puas hlwb ^[1].

Xaus

Raws li mitochondrial-derived peptide, MOTs-C activates signaling pathways zoo li AMPK los tswj cov piam thaj thiab lipid metabolism, txhawb kev hloov pauv cov rog dawb-rau-xim av, thiab txhim kho insulin tsis kam thiab rog, muab cov lus qhia kho tshiab rau cov kab mob metabolic. Nws txhim kho kev sib txawv ntawm osteoblast, suppresses osteoclast tsim, sib npaug ntawm cov pob txha metabolism, thiab txhawb nqa kev noj qab haus huv ntawm pob txha. Nws tswj cov leeg nqaij sib txawv thiab tiv thaiv atrophy, tuav lub peev xwm rau kev cuam tshuam hauv cov leeg mob. MOTs-C nthuav tawm cov koom haum muaj zog txog kev tawm dag zog: kev tawm dag zog txhawb nqa nws cov lus qhia, thiab nws kho kom haum rau cov txiaj ntsig kev noj qab haus huv. MOTs-C kuj tseem ua lub luag haujlwm hauv kev ncua kev laus thiab cov txheej txheem cuam tshuam.

Hais Txog Tus Sau

Cov ntaub ntawv hais saum toj no yog txhua yam tshawb fawb, kho thiab sau los ntawm Cocer Peptides.

Scientific Journal Author

Ning Ran yog tus kws tshawb fawb koom nrog Carlson College of Veterinary Medicine ntawm Oregon State University. Nws txoj haujlwm kev kawm nthuav dav molecular biology thiab tshuaj txhais lus, nrog rau kev tsom mus rau cov tswv yim kho mob rau cov kab mob neuromuscular. Ran tau koom nrog ntau cov ntawv tshaj tawm hauv cov ntawv txheeb xyuas cov phooj ywg, ua rau muaj kev nkag siab txog kev cuam tshuam ntawm molecular hauv cov qauv kab mob. Nws cov kev xav tau kev tshawb fawb suav nrog kev txhim kho thiab kev siv peptide-conjugated oligonucleotides, nrog rau kev tshawb nrhiav cov peev xwm kho mob ntawm mitochondrial-derived peptides. Ning Ran tau teev nyob rau hauv kev siv ntawm cov ntaub ntawv pov thawj [6].

▎ Cov Lus Qhia Tseem Ceeb

[1] Gao Y, Wei X, Wei P, et al. MOTs-C Functionally Prevents Metabolic Disorders. Metabolites 2023; 13(1).DOI: 10.3390/metabo13010125.

[2] Wang Z, Yang L, Xu L, Liao J, Lu P, Jiang J. Central thiab peripheral mechanism ntawm MOTs-C attenuates mob hypersensitivity nyob rau hauv nas qauv ntawm inflammatory mob. Neurological tshawb fawb 2024; 46(2): 165-177.DOI: 10.1080/01616412.2023.2258584.

[3] Benayoun BA, Lee C. MOTs-C: A Mitochondrial-Encoded Regulator of the Nucleus. Bioessays 2019; 41(9): e1900046.DOI: 10.1002/bies.201900046.

[4] Shen Z, Lu P, Jin W, et al. MOTs-C Txhawb nqa Glycolysis ntawm AMPK-HIF-1α-PFKFB3 Txoj Kev rau Ameliorate CPB-induced Lung Injury. American Journal of Respiratory Cell thiab Molecular Biology 2025. 10.1165/rcmb.2024-0533OC.

[5] Zhang Y, Zhang J, Zhang Y, et al. Mitochondrial-Derived Peptide MOTs-C Alleviates Radiation Pneumonitis ntawm Nrf2-Dependent Mechanism. Antioxidants 2024; 13. https://api.semanticscholar.org/CorpusID:269876125.

[6] Ran N, Lin C, Leng L, et al. MOTs-C txhawb nqa phosphorodiamidate morpholino oligomer uptake thiab ua tau zoo hauv cov nas dystrophic. Embo Molecular Tshuaj 2021; 13(2): e12993.DOI: 10.15252/emmm.202012993.

[7] García-Benlloch S, Revert-Ros F, Blesa JR, Alis R. MOTs-C txhawb nqa cov leeg sib txawv hauv vitro. Peptides 2022; 155: 170840.DOI: 10.1016/j.peptides.2022.170840.

[8] Kumagai H, Coelho AR, Wan J, et al. MOTs-C txo cov myostatin thiab cov leeg nqaij atrophy. American Journal of Physiology-Endocrinology thiab Diabetes 2021; 320(4): E680-E690.DOI: 10.1152/ajpendo.00275.2020.

Tag nrho cov kab lus thiab cov ntaub ntawv ntawm cov khoom lag luam muab rau ntawm lub vev xaib no tsuas yog rau cov ntaub ntawv tshaj tawm kev tshaj tawm thiab cov hom phiaj kev kawm.  

Cov khoom muab rau hauv lub vev xaib no yog npaj tshwj xeeb rau kev tshawb fawb hauv vitro. Kev tshawb fawb hauv vitro (Latin: * hauv iav *, lub ntsiab lus hauv iav) yog ua los ntawm tib neeg lub cev. Cov khoom no tsis yog tshuaj, tsis tau txais kev pom zoo los ntawm US Food and Drug Administration (FDA), thiab yuav tsum tsis txhob siv los tiv thaiv, kho, lossis kho txhua yam mob, kab mob, lossis mob. Nws raug txwv nruj raws li txoj cai los qhia cov khoom no rau hauv tib neeg lossis tsiaj lub cev hauv txhua daim ntawv.