Motc 20mg we yu de du

▎ Motc Struktrɔ

▎ Motc Risach

Wetin na di risach bakgrɔn fɔ Motc?

di risεch bakgrכn fכ Motc kכmכt frכm invεstigeshכn dεm pan di rol we maytochכndrial DNA de ple fכ mεtabolik hεlth εn ol. as di כndastandin fכ di maytochכndrial fכnshכn de dip, dεn dכn diskכv se maytochכndria nכto nכmכ di sεntrכm fכ enεji mεtabolism bכt dεn de tek pat bak pan sεlyul kכmyunikeshn εn signal transdyushכn. bay we dεn de aktibכt di AMPK path, dεn de involv insay glukכs εn lipid mεtabolism, we kכl mεtabolik sik dεm lεk mεtabolism εn fat, εn dεn de ol prכmis as nyu tεrapi tכgεt fכ dεn kכndishכn dεm ya. we dεn gi di asosieshכn bitwin di maytochכndrial fכnshכn εn difrεn sik dεm, dεn bin aplay Motc bak insay kכndishכn dεm lεk krεse εpataytis B εn ovarian kεnsar. Risach sho se i kin ple big pat pan di vayral infεkshכn prכsεs dεm. εksεsayz de promuot di sεntesis εn εksprεshכn fכ Motc insay di mכtalman bכdi, we de mek di mכsul mεtabolism, fכshal pכrfomans, εn כvala bכdi fכnshכn, de gi pruf fכ εksεsayz-bεys anti-aging stratεji dεm εn i de εkspεnd di skop fכ Motc risεch.

Wetin na di mɛkanism fɔ akshɔn fɔ Motc?

Aktivεshכn כf di AICAR-AMPK signal path: 

Motc de fכs fכ du in fysiolojikal fכnshכn dεm bay we i de aktibכt di AICAR-AMPK signal path. i de disrupt di folate-methionine saykl insay di sεl dεm, we de aktibכt di AICAR-AMPK signal path. fכ egzampl, insay di fysiolojikal prכsεs dεm lεk fכ impruv insulin rεsistεns εn fכ mek i nכ fat, di aktibכshכn fכ dis path de ple wan imכtant rol. bay we i de aktibכt dis path, Motc kin rεgεl sεlyul εnεji mεtabolism, εnhans sεlyul כptek εn yutilizeshכn fכ glukכs, we de rεgεl sistεmik mεtabolik homכstasis ^[1,2]..

intarakshכn wit spεsifi k signal path dεm εn jin dεm: 

insay mכsul sεl dεm, Motc de intarakt wit signal transdyushכn εn transkripshכn aktibכt 3 (STAT3) tru in YIFY domεn in putativ Src-homologous 2 (SH2) binding mכtif, we de ridyus STAT3 in transkripshכnal aktvכti εn εnhans myotub fכmeshכn. insay rεdyushכn nyumonitis, Motc de εliviet di lכng tisu dεm, inflameshn, εn כksidεtiv strεs bay we i de inkrεs nyuklia fכktכ E2-rεlatεd fכktכ (Nrf2) lεvεl dεm εn protεkt in nyuklia translכkeshכn, we de protεkt di maytochכndrial fכnshכn. apat frכm dat, Motc de du difrεn fysiolojikal fכnshכn dεm bay we i de rεgεl di εksprεshכn fכ jin dεm lεk GLUT4, STAT3, εn IL-10 ^[3]..

rεgulεshכn fכ di mεtabolik path dεm: 

Motc de tek pat pan di rεguleshכn fכ difrεn imכtant mεtabolik prכsεs dεm, inklud glukכs mεtabolism, lipid mεtabolism, εn bon mεtabolism, tru כtokrin εn parakrin mεkanism dεm. insay glukoz mεtabolism, i de mek insulin rεsistεns εn i de rεgεl di blכd glukכs lεvεl; insay lipid mεtabolism, i de inkrεs di brawn fεt tεmכjεnεsis, i de mek di wayt fεt brawn, εn i de mek i nכ fat εn di lipid mεtabolism dizכrd; insay bon mεtabolism, i de protεkt di כstioblast proliferashכn, difrεns, εn minralayzεshכn, i de inhεbit כsteoklast jεnereshכn, εn i de rεgεl di bon mεtabolism εn bon rimכdelin ^[4,5]..

Figure 1 Mekanism ɛn di wok we Motc de du ^[6]..

Wetin na di wok ɛn aplikeshɔn dɛn we Motc de du?

Di wok dɛn we Motc de du

rεgεdyushכn ifekt dεm pan mεtabolism: 

Motc kin impruv glukoz εn lipid mεtabolism na di bכdi. insay glukoz mεtabolism, i de ridyus insulin rεsistεns, i de εp fכ mek di tayp 2 mεtabolism nכ de, εn i de mek di sεl dεm tek εn yutilizeshכn efyushכn fכ glukכs. insay di lipid mεtabolism, i de inkrεs di brawn fεt tεmכjεnεsis, i de mek di wayt fεt brawn, we de rεgεl di lipid mεtabolism, i de mek i nכ fat, εn di lipid mεtabolik dizכrd dεm we de kכmכt wit am. i de ridyus di insidεns fכ nכn-alkohol fεt liva sik εn i de rεgεl di hεpatik lipid mεtabolism ^{[2] .}.

di ifekt dεm pan di sεl dεm we de wok: 

i de mek di maytochכndria wok fayn εn i de protεkt di sεl dεm frכm damej. fכ egzampl, insay nyumonia we di rεdyushכn de mek, i de ridyus di maytochכndrial dεm we de na di lכng εpitεlial sεl dεm, i de dכn di sεl apoptosis, εn i de mek di sεl dεm wok nכmal. insay pankrεas sεl dεm, Motc de infכlכw di sekreshכn εn εksprεshכn fכ insulin εn glukagon, we de rεgεl pankrεas sεl fysiolכji, εn i de afekt sεl viabiliti εn apoptosis bak ^[4,5]..

Di tin dɛn we kin apin to di mɔsul ɛn bon dɛn: 

insay di mכsul dεm, Motc de protεkt di mכsul progenitor sεl dεm difrεns, i de inkrεs di myotube fכmeshכn, εn i de protεkt di mכsul sεl dεm frכm di damej we intalyukin-6 (IL-6) de mek, we kin mek di mכsul dεm nכ atrofi. we i kam pan bon dεm, i de protεkt di proliferashכn, difrεns, εn minralayzεshכn fכ di כstioblast dεm, i de inhibit di כstioklast dεm fכ fכm, i de mεnten di bon mεtabolik bεlε, εn i de εp fכ delay di כstioporosis ^[1,5]..

Anti-inflammatory ɛn immunomodulatory ifɛkt dɛn: 

Motc de ridyus di sistεmik krכnik inflammatory rεspכns dεm εn i de rεgεl di imyun fכnshכn. insay inflammatory pen mכdel dεm, Motc de εliviet pen haypasεnsitiviti, rεdכks di rilis fכ inflammatory fכktכ dεm, εn de inhεbit di aktibכshכn fכ glial sεl dεm εn nyuron dεm, we de sho anti-inflammatory εn pen-rεliv ifekt dεm ^[3]..

Aplikeshɔn dɛn fɔ Motc

Efεkt dεm pan mεtabolik sik dεm: 

di rεgεdyushכn ifekt dεm we Motc gεt pan glukכs εn lipid mεtabolism de mek am wan nyu tεrapi tכgεt fכ mεtabolik sik dεm lεk tayp 2 mεtabolism, fεt, εn nכn-alkohol fεt liva sik ^[2]..

Prɛvenshɔn ɛn Tritmɛnt fɔ Mɔskul ɛn skel Disizin dɛn: 

di fayn fayn tin dεm we i de du pan di mכsul dεm εn bon dεm kin yus fכ prεvεnt εn trit sik dεm we de kכmכt frכm di mכsul dεm we de atrofi εn sik dεm we de na di skel lεk כstioporosis. fכ di sik pipul dεm we gεt mכsul atrofi, i kin impruv di mכsul fכnshכn bay we i de protεkt mכsul sεl difrεns εn inhεbit mכsul sεl apoptosis; fכ di sik pipul dεm we gεt כstioporosis, i kin rεgεl di bon mεtabolik bεlε, inkrεs di bon dεnsiti, εn i kin mek i nכ gεt εn trit כstioporosis ^[1,5]..

Protekshɔn fɔ di damej we di raytin de mek: 

Insay stεdi dεm pan rεdyushכn nyumonitis, Motc dכn sho protεktiv ifekt dεm εgεst lכng rεdyushכn damej. Dɛn kin yuz am we dɛn de du redio tɛrapi fɔ protɛkt di nɔmal tisu dɛn, fɔ ridyus di damej we di tisu dɛn kin du we redyushɔn kin pwɛl, ɛn fɔ mek di redio tɛrapi wok fayn ^{[2] .}.

Tritmɛnt fɔ sik dɛn we kin mek pɔsin gɛt inflammatory: 

bays pan in anti-inflammatory ifekt, dεn kin yuse Motc fכ trit inflammatory sik dεm lεk inflammatory pen, we de gi nyu dairekshכn fכ trit dεn kayn kכndyushכn dεm ya ^[3]..

Dɔn

as pεptida we kכmכt frכm di maytochכndrial, Motc kin aktibכt signal path dεm fכ rεgεl glukכs εn lipid mεtabolism, impruv insulin rεsistεns, εn ridyus di risk fכ mεtabolik sik dεm; i kin mek bak di mכsul dεm εn bon dεm wok fayn, i kin mek di mכsul dεm atrofi εn כstioporosis; εn i gεt anti-inflammatory εn sεl-protektiv fכnshכn dεm, we de ple rol fכ rεdyushכn damej protεkshכn εn trit inflammatory sik dεm.

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

Wan, Yanmin gɛt fɔ du wit difrɛn ɔganayzeshɔn dɛn we gɛt nem, we inklud ɔspitul, risach sɛnta, yunivasiti, ɛn ɛntapraiz dɛn lɛk Linping Hosp Integrated Tradit Chinese & Western M, Shanghai Sci Tech Inno Ctr Infect & Immun, Yunnan Agricultural University, ɛn ɔda wan dɛn In risach intɛres dɛn bɔku, mɔ i de pe atɛnshɔn pan di sɔbjɛkt kategori dɛn we na Immunology Science & Technology, Virology, ɛn Materials Science Kwɛstyɔn bɔt Kwɛstyɔn. Insay di fild fɔ Immunology Science & Technology, i de delve insay di mɛkanism ɛn aplikeshɔn fɔ di imyun sistɛm. In Vayrɔs risach de sɛnt pan di vayral kwaliti dɛm, transmishɔn, ɛn prɛvɛnshɔn. Insay di domɛyn fɔ Matirial Sayns Kɛmistri, i de kɔmit fɔ divɛlɔp matirial prɔpati ɛn di inovativ aplikeshɔn fɔ kemistri, we mek i bi wan notabɛl pɔsin wit impɔtant risach achivmɛnt dɛn na rilevɛns akademik fil dɛm. Wan, Yanmin de list in di rεfrεns כf saytεshכn [6].

▎ Saytayshɔn dɛn we gɛt fɔ du wit dis

[1] García-Bɛnlɔch S, Rɛvɛt-Ros F, Blɛsa JR, ɛn ɔda pipul dɛn. Motc de promuot mכsul difrεns in vitro[J]. Pεptid, 2022,155:170840.DOI:10.1016/j.pεptida.2022.170840.

[2] Zhang Y, Huang J, Zhang Y, ɛn ɔda pipul dɛn. di Maytochondrial-Dεriv Pεptid Motc de Aliviet Rεdyushכn Nyumonitis via wan Nrf2-Dipεndεnt Mεkanism[J]. Antioksidant, 2024,13.

[3] Wang Z, Yang L, Xu L, ɛn ɔda pipul dɛn. Sεntri εn pεrifεral mεkanism fכ Motc de atεnuet pen haypasεnsitiviti in wan mays mכdel fכ inflammatory pen[J]. Nyurolɔjik Risach, 2024,46(2):165-177.DOI:10.1080/01616412.2023.2258584.

[4] Bień J, Pruszyńska-Oszmałek E, Kołodziejski P, ɛn ɔda pipul dɛn. Motc de rεgεl pankrεas alfa εn beta sεl fכnshכn dεm in vitro[J]. Histokemistri ɛn Sɛl Bayoloji, 2024,161(6):449-460.DOI:10.1007/s00418-024-02274-0.

[5] Yi X, Hu G, Yang Y, ɛn ɔda pipul dɛn. di rol we Motc de ple na di rεguleshכn fכ di bon mεtabolism[J]. Frɔntiers in Fisiɔlɔji, 2023,14:1149120.DOI:10.3389/fphys.2023.1149120.

[6] Wan W, Zhang L, Lin Y, ɛn ɔda pipul dɛn. di mitochondria-derived peptide Motc: ifekt dεm εn mεkanism dεm we riliyt to strεs, mεtabolism εn ol[J]. J ɔ rnal ov Transleshɔnal Mɛdisin, 2023,21(1):36.DOI:10.1186/s12967-023-03885-2.

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.