Motc 10mg we yu de yuz

▎ Motc Struktrɔ

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

▎ Motc Risach

Wetin na di risach bakgrɔn fɔ Motc?

di maytochכndrion na imכtant sayt fכ enεji mεtabolism 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. Motc (maytochondrial opin ridin fכm fכ di 12S rRNA-c) na wan 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 Motc. stכdi dεn sho se Motc 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 Motc de kכlכs fכ di כkכrεshכn εn divεlכpmεnt fכ ol εn sik dεm we de kכmכt frכm di ej. fכ egzampl, di lεvεl fכ Motc na plasma de dכn wit di ej (Zheng Y, 2013). pan di sem tεm, dεn pruv se Motc bεnεfit fכ sik dεm we de kכmכt frכm di ej, lεk mεtabolism, kכdivaskyul sik dεm, כstioporosis, fכ fat afta mεnoposal, εn Alzaima sik ^[3]..

Wetin na di mɛkanism fɔ akshɔn fɔ Motc?

Rigulεt jin εksprεshכn: 

Motc kin du in fisiolכjik fכnshכn dεm bay we i de rεgεl jin εksprεshכn. fכ egzampl, i kin rεgεl di εksprεshכn fכ di jin dεm lεk GLUT4, STAT3, εn IL-10. Motc 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: 

Motc kin ridyus insulin rεsistεns εn mek di tayp 2 mεtabolism nכ de. di mεkanism fכ akshכn we i de du kin riliyt to di inhibishכn fכ myostatin. stכdi dεn dכn fכnshכn se di plasma Motc lεvεl nεgεtiv kכrεlat wit di myostatin lεvεl na di mכtalman bכdi. Motc kin impruv insulin sεnsitiviti bay we i de inhεbit di aktvכti fכ di כpstrim transkripshכn fכktכ FOXO1 εn i de ridyus di myostatin lεvεl ^[5]..

Fɔ mek di mɔsul dɛn difrɛn: 

insay mכsul sεl dεm, Motc de intarakt wit STAT3 tru wan putativ SH2 binding mכtif insay di YIFY rijyכn, we de ridyus di transkripshכnal aktvכti fכ STAT3, we de εnhans di myotube fכmeshכn. di wayl tayp Motc 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 stεyning we intalyukin-6 (IL-6) indyuz ^{[6] .}.

rεgulεt di maytochכndrial fכnshכn: 

Motc kin rεgεl di maytochכndrial mεtabolism. stכdi dεn sho se fכ trit mamal sεl dεm wit Motc 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 Motc tritmεnt. fכda risεch dεn fכnshכn se Motc 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 Motc fכ promuot GLUT4 translokeshכn εn glukכs כptek ^[7]..

Motc na wan pɔtɛnɛshɛl tritmɛnt target fɔ bɔku sik dɛn we gɛt fɔ du wit ol ol, lɛk nyurodijɛnɛreshɔn, ɔstioporosis, kadiovaskular sik, atrɔsklɛrosis, sarkopenia, tayp 2 mɛtabolism mɛlitus, ɛn fat.

Sos:PubMed ^{[8] we dɛn pul am.}

Wetin na di aplikeshɔn dɛn fɔ Motc?

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

Rilayshɔnship wit ol pipul dɛn: 

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

Di mɛtabolism: . 

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

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

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

כstioporosis: Motc kin protεkt di proliferashכn, difrεns, εn minralayzεshכn fכ di כstioblast dεm, inhεbit di כstioklast jεnεsis, εn rεgεl di bon mεtabolism εn bon rimכdelin. εksεsayz kin ifektivli upregulate di εksprεshכn fכ Motc, bכt di spεsifi k mεkanism we εksεsayz de rεgεl Motc 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 (Motc) na pεptida we di maytochכndrial jεnom kכd, we gεt pכsitiv ifekt pan glukכs εn lipid mεtabolism, 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 εgzistin litεrachכ dεm pan di pכtεnshal rol we Motc 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: 

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

Fat ɛn mɔsul dɛn we nɔ de wok fayn: 

fat εn tayp 2 mεtabolism na mεtabolik sik dεm we kin bכku tεm wit sarkopenia εn mכsul dεm we nכ de wok fayn. Motc, as sistεmik כmon, de tek pat pan mεtabolik homכstasis. stכdi dεn dכn fכnshכn se di plasma Motc lεvεl nεgεtiv kכrεlat wit di myostatin lεvεl na di mכtalman bכdi. Motc kin mek di palmitik asid indyuz atrofi fכ difrεnt C2C12 myotub dεm εn ridyus di myostatin lεvεl na di plasma fכ di it-indyuz obes mays dεm. bay we i de inhεbit myostatin, Motc 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 brɔst kansa kin gɛt mɔ sik dɛn na dɛn at ɛn blɔd, dɛn mɛtabolism, ɛn dɛn kin fat, ɛn ɛksesaiz kin mek dɛn sayd ɛfɛkt ya nɔ bɔku. Motc gɛt ɛksɛsayz-mimik aktiviti ɛn i gɛt bɛnifit ifɛkt pan mɛtabolism ɛn ɛksɛsayz kapasiti. Stɔdi dɔn sho se 16 wik aerobik ɛn rɛsistɛns ɛksɛsayz intavɛnshɔn kin inkrisayz di Motc lɛvɛl pan pipul dɛn we nɔto Hispanik brɔst kansa, bɔt i nɔ gɛt ɛni impɔtant ifɛkt pan Hispanik brɔst kansa sɔvayv. di inkrεs pan di Motc lεvεl we dεn indyuz bay εksεsayz pan pipul dεm we nכto Hispanik brεst kεnsar kin riliyt to di impruvmεnt fכ insulin sεnsitiviti, we de ridyus di risk fכ kכmorbiditi ^[13]..

fכ kכnklud, as 16-amino asid polipεptida we di maytochכndrial jεnom de kכd, Motc de ple wan kכr rol insay di bכdi in mεtabolik rεguleshכn, strεs difεns, εn sik prεvεnshכn εn tritmεnt. i kin bכku bכku wan impruv di homכstasis fכ glukכs εn lipid mεtabolism, εnhans insulin sεnsitiviti, εn inhεbit di εksprεshכn fכ myostatin, ifektivli εliviet tayp 2 mεtabolism, fat, εn rilatεd mכsul atrofi. di sem tεm, bay we i de rεgεl di maytochכndrial bayojεnεsis εn fכs, Motc 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, Motc 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'.

Bɔt di pɔsin we rayt di buk

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. Motc: Wan prɔmis maytochכndrial-dεriv pεptida fכ tεrapi εksplכyshכn[J]. Frontiers in Ɛndokrinɔlɔji, 2023,14.DOI: 10.3389/fendo.2023.1120533.

[2] Boyu Y. Eksεsayz εn Motc de inkrεs di maytochכndrial-dεrivεd pεptida Motc 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. Motc, di mכst rεsεnt maytochכndrial dεrivεd pεptid in hכman εj-rεlatεd sik 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. Motc 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. Motc de ridyus myostatin εn mכsul atrofi signal[J]. Amɛrikan Jɔnal fɔ Fisiɔlɔji-Ɛndokrinɔlɔji ɛn Mɛtabolism, 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. Motc 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. Mitofushon de nid fכ Motc 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 Pεptid Motc, Mεtabolism, εn Aging-Rεlatεd Disizεs[J]. Mεtabolism & Mεtabolism Jכnal, 2023,47(3):315-324.DOI:10.4093/dmj.2022.0333.

[9] Wang M, Wang G, Pang X, ɛn ɔda pipul dɛn. Motc 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. di rol we Motc de ple na di rεguleshכn fכ di bon mεtabolism[J]. Frɔntiɛr in Fisiɔlɔji, 2023,14.DOI: 10.3389/fphys.2023.1149120.

[11] Zhang Z, Chen D, Du K, ɛn ɔda pipul dɛn. Motc: Na pכtεnshal anti-pulmonary fibrosis fכktכ we di maytochכndria dεm de kכmכt[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. Motc 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.