MOTs-C 10mg di wan dɛn we de wok

▎ MOT dɛn-CSstrukchɔ

Sos: PubChem

Sikyɔn: MRWQEMGYIFYPRKLR Molikul Fɔmula: C101H152N28O22S2 Molikul Weyt: 2174.6g/mol CAS Nɔmba: 1627580-64-6 PubChem CID: 146675088, ɛn di ɔda wan dɛn Sinonim dɛn: UNII-A5CV6JFB78

▎ MOTs-C Risach

Wetin na di risach bakgrɔn fɔ MOTs-C?

di maytochכndrion na imכtant sayt fכ enεji dayabεtis insay sεl dεm. Fɔ lɔng tɛm naw, sayɛnsman dɛn dɔn de du bɔku ɛn dip risach bɔt di we aw di maytokɔndria dɛn tan ɛn aw i de wok. insay dis prכsεs, dεn dכn no sכmtεm se di maytochכndria nכ de nכmכ de ple wan kכl rol fכ prodyuz enεji bכt i kin tek pat pan כda fysiolojikal prכsεs dεm fכ di sεl dεm tru sכm mεkanism dεm we dεn nכ no.

wit di kכntinyu fכ risεch tεknכlכji dεm, spεshal wan di divεlכpmεnt fכ jεnomiks εn proteomiks tεknכlכji dεm, i dכn bi posεbul fכ fכnshכn nyu mכlikul dεm we rilet to maytochכndria. MOTs-C (maytochondrial opin ridin fכm fכ di 12S rRNA-c) na di mitochondria-dεriv pεptida we di 12S rRNA rijyכn fכ di mitochondrial jεnom de kכd ^[1]..

tru dip analisis fכ di maytochכndrial jεnom, sayɛnsman dεn dכn fכnshכn sכm sכm sכm opin ridin fכm dεm (sORF dεm), we kin kכd sכm pεptida dεm wit spεsifi k fכnshכn dεm. Afta ɔda risach ɛn verifyeshɔn, dɛn bin no MOTs-C. stכdi dεn dכn fכnshכn se MOTs-C de εksprεs insay difrεn tisu dεm na mכtalman εn animal. i de mεnli akt pan di skel mכsul dεm tru di bכdi, we de mek di glukכs tek εn yutilizeshכn bכku, we de mek di insulin rεsistεns εn rεgεl mεtabolik bεlε ^{[2] .}.

Wit di dip we di risach de dip, dεn fכnshכn se chenj dεm na di εksprεshכn fכ MOTs-C gεt klos to di כkכrεshכn εn divεlכpmεnt fכ ol εn sik dεm we de kכmכt frכm di ej. fכ egzampl, di lεvεl fכ MOTs-C na plasma de dכn wit di ej (Zheng Y, 2013). Na di sem tɛm, dɛn dɔn pruv se MOTs-C fayn fɔ sik dɛn we gɛt fɔ du wit di ej, lɛk dayabitis, sik dɛn we gɛt fɔ du wit at ɛn blɔd, ɔstioporosis, fat we pɔsin kin fat afta i dɔn pas 40 ia, ɛn Alzaima sik ^[3]..

Wetin na di mεkanism fכ akshכn fכ MOTs-C?

Rigulεt jin εksprεshכn: 

MOTs-C kin du in fisiolכjik fכnshכn dεm bay we i de rεgεl jin εksprεshכn. fכ egzampl, i kin rεgεl di εksprεshכn fכ jin dεm lεk GLUT4, STAT3, εn IL-10. MOTs-C mεnli de εksyεrt in ifekt bay we i de aktibכt di AICAR-AMPK signal path εn disrupt di folate-methionine saykl insay sεl dεm ^[4]..

Fɔ mek di insulin rɛsistɛns bɛtɛ: 

MOTs-C kin ridyus insulin rɛsistɛns ɛn mek yu nɔ gɛt tayp 2 dayabitis. di mεkanism we i de aks kin riliyt to di inhibishכn fכ myostatin. stכdi dεn dכn fכnshכn se di plasma MOTs-C lεvεl nεgεtiv kכrεlat wit di myostatin lεvεl na di mכtalman bכdi. MOTs-C kin impruv insulin sεnsitiviti bay we i de inhεbit di aktvכti fכ di כpstrim transkripshכn fכktכ FOXO1 εn ridyus di myostatin lεvεl ^[5]..

Fɔ mek di mɔsul dɛn difrɛn: 

insay mכsul sεl dεm, MOTs-C de intarakt wit STAT3 tru wan putativ SH2 binding mכtif na di YIFY rijyכn, we de ridyus di transkripshכnal aktvכti fכ STAT3, we de εnhans di myotube fכmeshכn. di wayl tayp MOTs-C pεptida kin inkrεs di myotube fכmeshכn fכ di hכman (LHCN-M2) εn maws (C2C12) mכsul progenitor sεl dεm εn protεkt mכsul sεl dεm frכm di rεdukshכn fכ nyuklia myogenin stεin we intalyukin-6 (IL-6) indyuz ^[6]..

rεgεlεt di maytochכndrial fכnshכn: 

MOTs-C kin rεgεl di maytochכndrial dayabεtis. stכdi dεn sho se fכ trit mamal sεl dεm wit MOTs-C i kin inkrεs di protin lεvεl dεm fכ di maytochכndrial bayojεnεsis mak dεm TFAM, COX4, εn NRF1, bכt fכ fכlכ saytכmetri analisis sho se di nכmba fכ di maytochכndria dεm de dכn shap afta MOTs-C tritmεnt. fכda risεch dεn fכnshכn se MOTs-C kin sinkrכn aktibכt maytochכndrial fכs εn inkrεs di protin lεvεl dεm fכ tu GTPase dεm, OPA1 εn MFN2, we implεnt fכ di fכs fכ di mamal maytochכndria. fכ inhibit dεn tu GTPase dεm ya כ kכnכk dכn MFN2 tru siRNA i go εliminet di abiliti fכ MOTs-C fכ promuot GLUT4 translokeshכn εn glukכs כptek ^[7]..

MOTs-C na wan pɔtɛnɛshɛl tritmɛnt target fɔ bɔku sik dɛn we gɛt fɔ du wit ol ol, lɛk nyurodijɛnɛreshɔn, ɔstioporosis, kadiovaskular sik, atɛrosklɛrosis, sarkopenia, tayp 2 dayabitis, ɛn fat.

Sos:PubMed ^{[8] we dɛn pul am.}

Wetin na di aplikeshɔn dɛn fɔ MOTs-C?

Fɔ mek di sik dɛn we pɔsin kin gɛt we i ol, bɛtɛ

Rilayshɔnship wit ol pipul dɛn: 

MOTs-C na pεptida we kכmכt frכm maytochכndria, εn chenj dεm na in εksprεshכn de kכlכs fכ di כkכrεshכn εn divεlכpmεnt fכ ol εn sik dεm we de kכmכt frכm di ej. As pipul dεn de ol, di lεvεl fכ MOTs-C de dכn. stכdi dεm dכn fכnshכn se εksεsayz gεt sכm impak pan di εksprεshכn fכ MOTs-C, εn MOTs-C kin mεdiet di anti-aging ifekt fכ εksεsayz ^[3]..

shuga: 

MOTs-C kin impruv di bכdi in glukכs εn lipid dayabεtis, protεkt di maytochכndrial fכnshכn insay sεl dεm, εn ridyus di sistεmik krכnik inflammatory rεspכns. Fɔ di wan dɛn we gɛt dayabitis, di lɛvɛl fɔ MOTs-C na plasma de dɔŋ. MOTs-C kin rεgεl mεtabolik homכstasis bay we i de aksεlεrayt glukכs כptek εn impruv insulin sεnsitiviti, εn i gεt fayn ifekt fכ prεvεnt tayp 2 dayabεtis ^[8]..

Di sik dɛn we kin apin to di at ɛn di blɔd: 

di kadyak strכkchכral rimodεlin εn disfכnkshכn na kכmכn kכmplikεshכn dεm fכ dayabitis, bכku tεm kin mek i gεt siriכs kכdivaskyul ivent dεm. MOTs-C kin impruv vaskulכr εndoteyl fכnshכn εn na nyu tεrapi tכgεt fכ kכdivaskyul kכmplikεshכn dεm fכ dayabitis. stכdi dεn sho se MOTs-C kin ripεr di mayokardial maytochכndrial dεmεj insay dayabεtik rat dεm εn protεkt di kadyak sistolik εn dayastolik fכnshכn dεm ^[9]..

כstioporosis: MOTs-C kin mek di כstioblast dεm proliferashכn, difrεns, εn minralayzεshכn, inhεbit di כstioklast jεnεsis, εn rεgεl di bon dayabεtis εn bon rimכdelin. εksεsayz kin ifektivli upregulate di εksprεshכn fכ MOTs-C, bכt di spεsifi k mεkanism we εksεsayz de rεgεl MOTs-C insay bon dεm stil nכ klia ^[10]..

Ɔda sik dɛn

Pɔlmonari fibrosis: . 

Pulmonary fibrosis na siriɔs lכng sik wit pwεl prכgnosis, εn in etiology εn pathogenesis stil nכ klia. di maytochכndrial opin ridin fכm fכ 12S rRNA-c (MOTs-C) na pεptida we di maytochכndrial jεnom kכd, we gεt pכsitiv ifekt pan glukכs εn lipid dayabεtis, sεlyul εn maytochכndrial homכstasis, εn di rεdukshכn fכ di sistεmik inflammatory rεspכns, εn i kin bi pכtεnshal εksεsayz mεtik. dis rivyu de aim fכ komprεhεnsivli analכz di litεrachכ dεm we de naw pan di pכtεnshal rol we MOTs-C de ple fכ impruv di divεlכpmεnt fכ pulmonary fibrosis εn fכ no spεsifi k tεrapi tכgεt fכ fכs tritmεnt stratεji dεm ^[11]..

Duchenne mכskul dεstrofi: 

MOTs-C na maytochondria-dεriv bayoaktiv pεptida wit inhεrent mכsul-tכgεt prכpati dεm, we kin inkrεs di glycolytic flux εn enεji prodakshכn kapasiti fכ distrofik mכsul dεm in vitro εn in vivo, we de εnhans di כptek εn aktvכti fכ fכsfonodiamidayt mכrfolino oligomers (PMO) in mdx mays dεm. lכng tεm ripit administreshכn fכ MOTs-C εn PMO kin indyuz di εksprεshכn fכ di tεrapi lεvεl dεm fכ distrofin insay di pεrifεral mכsul dεm, impruv di mכsul fכnshכn εn patכlayzm fכ mdx mays, εn i nכ gεt nכ klia tכksisiti ^[12]..

Fat ɛn mɔsul dɛn we nɔ de wok fayn: 

Fat ɛn tayp 2 dayabitis na mɛtabolik sik dɛm we kin gɛt fɔ du wit sarkopenia ɛn mɔsul dɛm we nɔ de wok fayn. MOTs-C, as sistεmik כmon, de tek pat pan mεtabolik homכstasis. stכdi dεn dכn fכnshכn se di plasma MOTs-C lεvεl nεgεtiv kכrεlat wit di myostatin lεvεl na di mכtalman bכdi. MOTs-C kin mek di palmitik asid indyuz atrofi fכ difrεnt C2C12 myotub dεm εn ridyus di myostatin lεvεl insay di plasma fכ di it-indyus fכ fat mays dεm. bay we i de inhεbit myostatin, MOTs-C kin bi wan pכtεnshal tritmεnt fכ skel mכsul atrofi we kכz fכ insulin rεsistεns εn כda mכsul atrofi fεnotayp dεm inklud sarkopenia ^[5]..

Risk fɔ mɛtabolik sik dɛn pan pipul dɛn we dɔn gɛt bɔdi kansa: 

Uman dɛn we dɔn gɛt tritmɛnt fɔ dɛn brɔst kansa kin gɛt mɔ sik dɛn we de ambɔg dɛn at ɛn blɔd, dayabitis, ɛn fat, ɛn ɛksesaiz kin mek dɛn bad bad tin ya nɔ apin. MOTs-C gɛt ɛksɛsayz-miks aktiviti ɛn i gɛt bɛnifit ifɛkt pan dayabitis ɛn ɛksɛsayz kapasiti. Stɔdi dɔn sho se 16 wik aerobik ɛn rɛsistɛns ɛksɛsayz intavɛnshɔn kin inkrisayz di MOTs-C lɛvɛl pan pipul dɛn we nɔto Hispanik brɔst kansa, bɔt i nɔ gɛt ɛni impɔtant ifɛkt pan Hispanik brɔst kansa sɔvayva dɛn. di inkrεs pan di MOTs-C lεvεl we dεn indyuz bay εksεsayz pan di wan dεm we nכ de pan brεst kεnsar kin riliyt to di impruvmεnt fכ insulin sεnsitiviti, we de ridyus di risk fכ kɔmכrbiditi ^[13]..

fכ kכnklud, as 16-amino asid polipεptida we di maytochכndrial jεnom de kכd, MOTs-C de ple wan kכr rol insay di bכdi in mεtabolik rεguleshכn, strεs difεns, εn sik prεvεnshכn εn tritmεnt. i kin bכku bכku wan fכ impruv di homכstasis fכ glukכs εn lipid dayabεtis, εnhans insulin sεnsitiviti, εn inhεbit di εksprεshכn fכ myostatin, we de εfεktiv wan fכ εliviet tayp 2 dayabεtis, fat, εn rilatεd mכsul atrofi. di sem tεm, bay we i de rεgεl di maytochכndrial bayojεnεsis εn fכs, MOTs-C de εnhans di sεl in antioksidant kapasiti εn i de inhεbit di inflammatory rεspכns, we de sho tεrapi pכtεnshal fכ krεse sik dεm lεk kכdivaskyul sik dεm, כstioporosis, εn pulmonary fibrosis. patikyula imכtant, as di kכl mεdiate fכ di maytochכndria-nyuklios kכmyunikeshn, MOTs-C kin simul di ifekt dεm we εksεsayz de gi εn delay di ol prכsεs. in lεvεl de nεgεtiv kכrεlat wit di sik dεm we de kכmכt wit di ej, εn εksojen supliment kin rivεs mεtabolik dizכrd dεm εn inhεbit di vayral rεplikshכn. dεn kכl am di 'maytochondrial כmon'.

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Di tin dɛn we wi dɔn tɔk bɔt, na ɔl di tin dɛn we Cocer Peptides dɔn du risach, ɛdit ɛn kɔmpilayt.

Sayɛns Jɔnal Author

Dieli-Conwright CM na masta sabi bukman we gɛt bɔku inflɔɛns pan di intadisiplinari fild fɔ ɔnkɔlɔji ɛn ɛksɛsayz sayɛns. Naw, i de wok as asosiet prɔfɛsɔ fɔ mɛrɛsin na Havad Mɛdikal Skul ɛn di Dana-Farber Kansa Instityut ɛn i gɛt asosiet fakulti pozishɔn na di Dipatmɛnt fɔ Nutrishɔn na di Havad T. H. Chan Skul fɔ Pɔblik Ɛlth. Di risach we Dɔktɔ Dieli-Conwright bin du, de tɔk mɔ bɔt di impak we ɛksesaiz kin du to pipul dɛn we gɛt kansa, mɔ aw ɛksɛsayz kin mek dɛn bɔdi wok fayn, dɛn bon dɛn wɛlbɔdi, ɛn kwaliti layf fɔ di wan dɛn we gɛt kansa. In akademik bakgrɔn de kɔba bɔku tin dɛn lɛk bayoloji, kinesiɔlɔji, pɔblik wɛlbɔdi, ɛn bayɔkinɛsiɔlɔji. I dɔn in stɔdi na institiushɔn dɛn lɛk Kalifɔnia Stet Yunivasiti, Nɔtridj, ɛn di Yunivasiti ɔf Sawt Kalifɔnia ɛn i dɔn in postdɔkta risach na Siti ɔf Hop Nashɔnal Mɛdikal Sɛnta. Dɛn dɔn rayt bɔku tin dɛn bɔt di risach we Dɔktɔ Dieli-Conwright dɔn du na difrɛn akademik jɔnal dɛn, ɛn in wok gɛt fɔ du wit bɔku tin dɛn lɛk pɔblik wɛlbɔdi biznɛs, it, di at ɛn blɔd sistɛm, ɛn di we aw dɛn de du dɛn at, ɛn dis de gi impɔtant sayɛns pruf fɔ di rihabiliteshɔn ɛn wɛlbɔdi manejmɛnt fɔ di wan dɛn we gɛt kansa. Dieli-Conwright CM de list in di rεfrεns כf saytεshכn [13].

▎ Saytayshɔn dɛn we gɛt fɔ du wit dis

[1] Zheng Y, Wei Z, Wang T. MOTs-C: Wan prɔmis maytochכndrial-dεrivεd pεptida fכ tεrapi εksplכyshכn[J]. Frontiers in Ɛndokrinɔlɔji, 2023,14.DOI: 10.3389/fendo.2023.1120533.

[2] Boyu Y. Eksεsayz εn MOTs-C inkrεs di maytochכndrial-dεrivεd pεptida MOTs-C εksprεshכn εn impruv insulin rεsistεns via AMPK/PGC-1α path[D]. Medikal Yunivasiti, 2019.10.27652/d.cnki.gzyku.2019.001531.

[3] Mohtashami Z, Singh M. K., Salimiaghdam N, ɛn ɔda pipul dɛn. MOTs-C, di Mכst Risεnt Maytochכndrial Dεriv Pεptid in Human Aging εn Ej-Rεlatεd Disiz dεm[J]. Int ɛ rnash ɔ nal J ɔ rnal ɔ f Mɔlikul Sayns, 2022,23(19).DOI:10.3390/ijms231911991.

[4] Gao Y, Wei X, Wei P, ɛn ɔda pipul dɛn. MOTs-C Fכnshכnal Prεvεnt Mεtabolik Dizכrd[J]. Mεtabolayt, 2023,13(1).DOI:10.3390/mεtabo13010125.

[5] Kumagai H, Coelho A. R., Wan J, ɛn ɔda pipul dɛn. MOTs-C de ridyus myostatin εn mכsul atrofi signal[J]. Amɛrikan Jɔnal fɔ Fisiɔlɔji-Ɛndokrinɔlɔji ɛn dayabitis, 2021,320(4): E680-E690.DOI: 10.1152/ajpendo.00275.2020.

[6] Garsia Bɛnlɔch S, Fransisko R. R., Rafaɛl Blɛsa J, ɛn ɔda pipul dɛn. MOTs-C de promuot mכsul difrεns in vitro[J]. Pεptid, 2022,155.DOI: 10.1016/j.pεptida.2022.170840.

[7] Bhullar KS, Shang N, Kerek E, ɛn ɔda pipul dɛn. Mitofushכn de nid fכ MOTs-C indyuz GLUT4 translokeshכn[J]. Sayntis Ripɔt, 2021,11(1).DOI: 10.1038/s41598-021-93735-2.

[8] Kong BS, Lee C, Cho Y M. Maytochondrial-Encoded Pεptida MOTs-C, dayabεtis, εn Aging-Rεlatεd Disizεs[J]. dayabitis & dayabitis Jɔnal, 2023,47(3):315-324.DOI:10.4093/dmj.2022.0333.

[9] Wang M, Wang G, Pang X, ɛn ɔda pipul dɛn. MOTs-C de ripair mayokardial damej bay we i de inhεbit di CCN1/ERK1/2/EGR1 path in dayabεtik rat[J]. Frontiers in Nutrishɔn, 2023,9.DOI: 10.3389/fnut.2022.1060684.

[10] Yi X, Hu G, Yang Y, ɛn ɔda pipul dɛn. Rol we MOTs-C de ple na di rεguleshכn fכ bon dayabεtis[J]. Frɔntiɛr in Fisiɔlɔji, 2023,14.DOI: 10.3389/fphys.2023.1149120.

[11] Zhang Z, Chen D, Du K, ɛn ɔda pipul dɛn. MOTs-C: na pכtεnshal anti-pulmonary fibrosis fכktכ we dεn kכmכt frכm maytochכndria[J]. Mitochondrion, 2023,71:76-82.DOI:10.1016/j.mito.2023.06.002.

[12] Ran N, Lin C, Leng L, ɛn ɔda pipul dɛn. MOTs-C de promuot fכsfכrodiamidεt mכfכlino כligomεr כptek εn efikכs in distrofik mays[J]. Embo Mɔlikul Mɛdisin, 2021,13(2).DOI:10.15252/emmm.202012993.

[13] Dieli-Kɔnrayt C. M., Natali S, K. ​​N. M., ɛn ɔda pipul dɛn. Efεkt כf aerobik εn rεsistεns εksεsayz pan di maytochכndrial pεptida MOTSc in Hispanik εn nכn-Hispanik brεst kεnsar sכvayva dεm.[J]. Kansa Risach, 2021,81(13).

ƆL DI ATIKUL ƐN PRODƆKT INFƆMƐSHƆN WE DƐN GI NA DIS WƐBSAYT NA FƆ ƆL FƆ DI INFƆMƐSHƆN ƐN FƆ EDYUKESHƆN.  

Di prɔdak dɛn we dɛn gi na dis wɛbsayt na fɔ in vitro risach nɔmɔ. in vitro risach (Latin: *in glas*, we min insay glas) dεn de du am ausayd mכtalman bכdi. Dɛn prɔdak ya nɔto famasitik, dɛn nɔ gɛt di aprɔval frɔm di US Food and Drug Administration (FDA), ɛn dɛn nɔ fɔ yuz dɛn fɔ protɛkt, trit, ɔ mɛn ɛni mɛrɛsin, sik, ɔ sik. Di lɔ nɔ gri fɔ mek dɛn put dɛn tin ya insay mɔtalman ɔ animal bɔdi ɛni we.