Cov txiaj ntsig zoo ntawm Exogenous Ketogenic Supplements Ntawm Cov Txheej Txheem Kev Laus Thiab Cov Hnub Nyoog Txog Cov Kab Mob Neurodegenerative Part 1

Abstract:

Lub neej expectancy ntawm tib neeg tau nce tsis tu ncua mus txog niaj hnub no, tab sis lawv txoj kev noj qab haus huv (kev noj qab haus huv) tsis tau kho kom zoo li qub. Txhawm rau txo cov kev kho mob loj, kev lag luam, thiab kev puas siab puas ntsws uas tshwm sim los ntawm qhov tsis sib xws, kev txhim kho kev noj qab haus huv yog tsim nyog uas ua rau ncua kev laus thiab kev loj hlob ntawm cov kab mob uas muaj hnub nyoog, yog li ua kom lub neej ntev.

Lub neej expectancy yog lub sij hawm ntev uas tus neeg muaj peev xwm ciaj sia nyob hauv lub ntiaj teb no, thiab nws cuam tshuam los ntawm ntau yam, xws li cov noob, kev noj haus, kev ua neej nyob, thiab lwm yam. Kev nco yog ib qho tseem ceeb tshaj plaws hauv tib neeg lub hlwb. Nws tuaj yeem pab peb tau txais cov ntaub ntawv, sau cov seem ntawm lub neej, thiab txiav txim siab kom raug. Puas muaj kev sib raug zoo ntawm ob?

Cov kev tshawb fawb tau pom tias muaj kev sib raug zoo ntawm lub neej expectancy thiab nco. Raws li cov neeg muaj hnub nyoog, lawv lub neej expectancy maj mam txo. Txawm li cas los xij, yog tias lawv tuaj yeem tswj tau qee qhov kev noj qab haus huv, xws li kev tawm dag zog thiab tswj kev noj zaub mov zoo, lawv lub neej expectancy tseem yuav txuas ntxiv mus. Ib yam li ntawd, tib neeg lub cim xeeb maj mam poob thaum lawv muaj hnub nyoog. Tab sis yog tias lawv tuaj yeem ua cov kauj ruam los txhim kho lawv txoj kev nco, lawv lub hlwb yuav nyob twj ywm thiab hloov tau yooj yim.

Raws li peb tau hais, kev sib raug zoo ntawm lub neej expectancy thiab nco yog complex, tab sis muaj ib qho kev sib txuas. Txawm hais tias tib neeg tsis tuaj yeem txiav txim siab lawv cov noob lossis lub neej expectancy, lawv tuaj yeem txhim kho lawv txoj kev noj qab haus huv thiab kev nco qab los ntawm lawv txoj kev siv zog. Piv txwv li, kev tawm dag zog, tswj kev pw tsaug zog zoo, thiab noj txiv hmab txiv ntoo thiab zaub tshiab, tuaj yeem pab txhim kho kev noj qab haus huv thiab lub hlwb. Tsis tas li ntawd, kev tawm dag zog lub hlwb tsis tu ncua, kawm cov txuj ci tshiab thiab kev paub, kev koom tes hauv kev sib raug zoo, thiab lwm yam tuaj yeem pab txhim kho kev nco.

Hauv cov ntsiab lus, muaj qhov sib txuas ntawm lub neej expectancy thiab nco, tab sis nws tsis yog kiag li. Txawm hais tias lub neej ntev npaum li cas, peb yuav tsum saib xyuas txhua hnub ntawm lub neej thiab txhim kho peb cov kev noj qab haus huv thiab kev zoo siab los ntawm kev noj qab haus huv thiab coj tus cwj pwm zoo. Cia peb txaus siab rau txoj kev taug kev ntawm lub neej ua ke! Nws tuaj yeem pom tias peb yuav tsum txhim kho kev nco, thiab Cistanche deserticola tuaj yeem txhim kho kev nco zoo vim Cistanche deserticola yog cov khoom siv tshuaj hauv Suav teb uas muaj ntau yam teebmeem, ib qho ntawm kev txhim kho kev nco. Kev ua tau zoo ntawm Cistanche deserticola los ntawm ntau yam khoom xyaw uas nws muaj, suav nrog tannic acid, polysaccharides, flavonoid glycosides, thiab lwm yam. Cov khoom xyaw no tuaj yeem txhawb lub hlwb kev noj qab haus huv los ntawm ntau txoj hauv kev.

Nyem paub 10 txoj hauv kev los txhim kho kev nco

Yog li, kev txhim kho cov cuab yeej kho tshiab los daws cov txheej txheem kev laus thiab cov kab mob cuam tshuam thiab ua kom lub neej expectancy yog ib lub ntsiab lus ntawm kev txaus siab. Nws yog dav lees paub tiasketosis (nce ntshav ketone lub cev qib, piv txwv li, -hydroxybutyrate) tuaj yeem tsim cov tshuaj tiv thaiv neuroprotective.

Ketosis-evoked neuroprotective teebmeem yuav ua rau kev txhim kho hauv kev noj qab haus huv thiab ncua kev laus thiab kev loj hlob ntawm cov kab mob cuam tshuam los ntawm kev txhim kho mitochondrial muaj nuj nqi, antioxidant thiab anti-inflammatory teebmeem, histone thiab non-histone acetylation, -hydroxybutyrylationof histones, modulation ntawm neurotransmitter systems thiab RNA kev ua haujlwm.

Kev tswj hwm ntawm cov tshuaj exogenous ketogenic tau raug pov thawj los ua ib txoj hauv kev zoo los txhawb thiab tswj kev noj qab haus huv ntawm cov zaub mov ketosis. Yog li ntawd, cov tshuaj ketogenic exogenous, xws li ketonesalts thiab ketone esters, tuaj yeem txo cov txheej txheem kev laus, ncua qhov pib ntawm cov kab mob uas muaj hnub nyoog, thiab txuas ntxiv lub neej los ntawm ketosis.

Qhov kev tshuaj xyuas no tsom mus rau cov ntsiab lus tseem ceeb ntawm cov txheej txheem kev laus thiab qee txoj hauv kev qhia hauv kev koom nrog (putative) muaj txiaj ntsig zoo ntawm exogenous ketogenic cov tshuaj ntxiv-evoked ketosis ntawm lifespan, aging txheej txheem, feem ntau cov kab mob neurodegenerative (Alzheimer's disease, Parkinson's disease, thiab amyotrophic). sclerosis), nrog rau kev kawm tsis zoo thiab kev nco ua haujlwm.

Cov ntsiab lus: ketogenic ntxiv; ketosis; kev laus; lub neej; kab mob neurodegenerative; kev kawm; nco.

1. Taw qhia

Cov txheej txheem kev laus ua rau qhov tsis tuaj yeem thim rov qab ntawm kev ua haujlwm ntawm lub cev ib txwm muaj (lub sijhawm ua haujlwm raws sijhawm poob) thiab cov kab mob muaj hnub nyoog. Nws tau raug pom tias ntau cov noob caj noob ces thiab ib puag ncig muaj peev xwm hloov kho cov haujlwm ntawm tes ua rau qhov tshwm sim ntawm kev laus, xws li cellular senescence, mitochondrial dysfunction, poob ntawm proteostasis, telomere attrition, deregulated nutrient sensing, stem cell exhaustion, thiab epitic 2. ].

Cov kev hloov no tuaj yeem tsim, piv txwv li, mob ntev thiab kev laus uas ua rau muaj kev pheej hmoo siab rau cov kab mob muaj hnub nyoog, xws li cov kab mob neurodegenerative (xws li, Alzheimer's disease), osteoporosis, kab mob plawv, mob qog noj ntshav, ntshav qab zib mellitus, sarcopenia, thiab osteoarthritis [1,2. ].Ib qho kev nce hauv ntiaj teb cov neeg laus tau kwv yees, raws li kwv yees li 9% ntawm cov neeg muaj hnub nyoog tshaj 65 xyoo xyoo 2019, thiab tus lej twg tau kwv yees nce mus txog kwv yees li 17% los ntawm 2050 [3,4].

Tib neeg txoj sia nyob tau nce ntxiv, vim yog cov cuab yeej kho mob ntau dua thiab zoo dua thiab txhim kho hauv kev ua neej nyob, tab sis kev noj qab haus huv ntawm cov neeg mob tsis tau txhim kho los ntawm tib lub zog. Yog li, feem ntau ntawm cov kab mob uas muaj hnub nyoog, xws li cov kab mob neurodegenerative tau nce ntxiv txhua xyoo [5,6] thiab qhov tshwm sim ntawm cov txheej txheem kev laus thiab cov kab mob cuam tshuam ua rau muaj kev kho mob loj heev, kev puas siab puas ntsws, thiab kev lag luam rau tib neeg [7].

Txhawm rau txo qhov tshwm sim tsis zoo ntawm cov txheej txheem kev laus thiab cov kab mob ntsig txog, yog li txo lawv qhov tsis zoo rau kev noj qab haus huv thiab kev lag luam, ntau cov tshuaj tau tsim tawm uas tab tom sim tshuaj kho mob.

Piv txwv li, rapamycin thiab nws cov analogues [8-10], metformin [11,12], sirtuin (SIRT) activators [13,14] thiab senolytics (rau tshem tawm cov hlwb senescent) [15] tuaj yeem hloov kho cov txheej txheem kev laus, thiab, qhov tshwm sim, nce lifespan thiab txo kev pheej hmoo rau cov kab mob uas muaj hnub nyoog.

Txawm li cas los xij, txhawm rau tiv thaiv, txo qis, thiab ncua sijhawm hnub nyoog txog cov txheej txheem thiab kab mob, kom ncua kev noj qab haus huv, thiab txhawm rau txhim kho lub neej zoo ntawm cov neeg laus, kev tsim cov tshuaj muaj kev nyab xeeb thiab zoo dua thiab cov cuab yeej kho mob yog xav tau. Exogenous ketogenic cov tshuaj ntxiv ( EKSs), xws li ketone esters (KEs, eg, R, S-1, 3-butanediol-acetoacetate diester), ketone ntsev (KSs, eg, Na+/K+- -hydroxybutyrate/ HBmineral ntsev), thiab nruab nrab cov saw triglycerides (MCTs / MCT cov roj uas muaj, piv txwv li, txog 60% caprylic triglyceride thiab 40% capric triglyceride) tau raug pov thawj zoo thaum siv ua ke nrog kev noj zaub mov zoo los txhawb thiab tswj cov ntshav ketone lub cev (ketosis) [ 16–20] ib.

Nws tau raug pom tias theem ntawm EKSs-induced ketosis tuaj yeem hloov pauv raws hnub nyoog thiab poj niam txiv neej [21]. Ketone lub cev (piv txwv li, HB thiab acetoacetate) tuaj yeem nkag mus rau hauv nruab nrab lub paj hlwb (CNS) ntawm monocarboxylate transporters thiab tuaj yeem siv rau ATP (adenosine triphosphate) synthesis ntawm Krebs voj voog hauv hlwb hlwb [22–25]. Nws tau raug pom tias EKSs tuaj yeem tsim tau sai (0.5-6 teev tom qab kev tswj hwm) thiab mob me mus rau nruab nrab [19,26–29] kho ketosis (kwv yees li 1–7 mM) [30,31].

Txhawm rau txhawb nqa kev kho mob ua rau muaj txiaj ntsig zoo, kev tswj hwm ntawm ntau qhov sib txawv ntawm EKSs yuav tsum tau rov ua dua ob peb hnub lossis txog li ob peb lub hlis nyob ntawm tus kab mob, koob tshuaj, thiab hom EKSs. Piv txwv li, kev tswj hwm ntawm 30 g MCT haus / hnub rau 6 lub hlis thiab 75 gKE / hnub rau 4 lub lis piam tuaj yeem ua rau muaj txiaj ntsig zoo rau cov neeg mob uas muaj kev paub tsis meej thiab mob ntshav qab zib hom 2, raws li [32,33].

Txawm li cas los xij, nws tau pom tias tsis yog cov no xwb, tab sis lwm cov EKSs yuav ua tau zoo thiab muaj kev nyab xeeb ketone lub cev ua ntej rau kev kho mob ntawm tib neeg los ntawm kev nce qib HB (ketosis) [29,32,34,35]. Nws tau ua pov thawj tias EKSs tau txais txiaj ntsig zoo thiab muaj kev nyab xeeb (nrog cov teebmeem me me, yog tias muaj) [19,26,28,29,33,36]. Tsis tas li ntawd, kev tswj hwm ntawm EKSs tuaj yeem hla ob qho tib si kev txwv kev noj zaub mov thiab kev tsis zoo ntawm cov khoom noj ketogenic (xws li, nephrolithiasis, cem quav, thiab hyperlipidemia) [37]. Yog li, kev tswj hwm ntawm EKSs yuav yog ib qho kev nyab xeeb thiab muaj txiaj ntsig zoo rau kev noj zaub mov ketogenic.

Nws kuj tau pom tias kev tswj hwm ntawm EKSs-tsim kev kho mob tuaj yeem ua rau muaj txiaj ntsig zoo rau cov kab mob CNS [34,38,39]. Piv txwv li, KEs, KSs, thiab MCT roj tuaj yeem tiv thaiv kev qaug dab peg thiab tiv thaiv kab mob vwm [36,40–42], anxiolytic cawv [26,43,44], rov tsim kho ntawm lub paj hlwb raug mob [45] thiab alleviating teebmeem onneurodegenerative kab mob (xws li Alzheimer's disease) [41,46–48].

Cov txiaj ntsig zoo no tau tshwm sim los ntawm ketosis-evoked neuroprotective teebmeem, piv txwv li, los ntawm kev txhim kho mitochondrial zog, txhim kho ATP qib, txo cov txheej txheem inflammatory, thiab txo qis oxidative stress [23,24,34,49,50]. Tsis tas li ntawd, ketone lub cev tuaj yeem hloov kho cov txheej txheem kev laus, uas ua rau lub neej ntev thiab ncua kev loj hlob ntawm cov kab mob uas muaj hnub nyoog, xws li cov kab mob neurodegenerative.

Nws tau raug pom tias tsis yog cov zaub mov ketogenic nkaus xwb, tab sis kuj tseem muaj kev tswj hwm ntawm EKSs tuaj yeem nce thiab tswj cov ntshav ketone lub cev qib [19,26–29], uas ketone lub cev, xws li HB, tuaj yeem txhawb kev laus [35,51,52] . Ntxiv mus, nws tau pom tias HB, ua ib qho endogenousligand molecule, tuaj yeem qhib lub hydroxycarboxylic acid receptor 2 (HCAR2 lossis GPR109Areceptor) [53,54]. HCAR2 receptors tau qhia tsis yog hauv macrophages nkaus xwb tab sis kuj nyob rau hauv lub hlwb hlwb, feem ntau hauv microglia, nrog rau astrocytes thiab neurons [54-56].

Yog li, HBmolecule ntawm, piv txwv li, HCAR2 receptors tuaj yeem hloov kho tsis tau tsuas yog lub cev nqaij daim tawv tab sis kuj muaj cov txheej txheem pathophysiological hauv lub hlwb uas txuas nrog kev laus thiab cov kab mob neurodegenerative [55,57,58]. Raws li cov ntaub ntawv, kev nce qib ntawm HB tuaj yeem yog qhov tseem ceeb ua rau muaj txiaj ntsig zoo rau kev laus, kev ua neej nyob, thiab cov kab mob muaj hnub nyoog tom qab kev tswj hwm ntawm EKSs. Tseeb tiag, nws tau pom tias HB txo qis cov tsos mob ntawm cov kab mob secretory phenotype (SASP) ntawm cov tsiaj nyeg [59] thiab txuas ntxiv lub neej ntawm C. elegans [60].

Yog li ntawd, hauv daim ntawv tshuaj xyuas no, peb tau tsom mus rau HB-generatedallleviating teebmeem. Txawm hais tias muaj pov thawj tsawg txhawb kev txo qis ntawm EKSs onlifespan, cov txheej txheem kev laus, thiab cov kab mob CNS cuam tshuam, peb tuaj yeem xav tias EKSs-evokedincrease hauv cov ntshav HB tuaj yeem hloov kho (txo) cov txheej txheem kev laus thiab txhim kho cov tsos mob ntawm cov kab mob hnub nyoog los ntawm lawv cov teebmeem neuroprotective, yog li ntawd yuav ncua ob qho tib si kev laus thiab kev loj hlob ntawm cov kab mob uas muaj feem xyuam thiab ua rau lub neej ntev.

Qhov kev tshuaj xyuas no tham txog cov ntsiab lus ntawm kev laus thiab kev tiv thaiv kev laus molecularmechanisms (txoj hauv kev) uas EKSs tuaj yeem siv tau lawv cov txiaj ntsig zoo ntawm lub neej, kev noj qab haus huv, kev laus, cov kab mob uas muaj hnub nyoog ntau tshaj plaws (Alzheimer's disease, Parkinson's disease thiab amyotrophic lateral). sclerosis), nrog rau kev kawm thiab kev nco.

2. Cov yam ntxwv tseem ceeb ntawm cov txheej txheem kev laus

Nws tau raug pom tias kev laus yog qhov kev pheej hmoo tshaj plaws rau qhov tshwm sim ntawm cov kab mob neurodegenerative [2]. Tseeb, raws li lub neej expectancy ntawm tib neeg nce, ntau thiab ntau tus neeg raug kev txom nyem los ntawm ntau hom kab mob neurodegenerative, xws li Alzheimer'sdisease [61].

Ntxiv mus, nws tau pom tias kev loj hlob thiab tshwm sim ntawm cov kab mob neurodegenerative feem ntau, Alzheimer's kab mob (xws li, tus cwj pwm los ntawm extracellular senile, amyloid- / A plaque thiab neurofibrillary tangle / hyperphosphorylated thiab misfolded Tau tsub zuj zuj hauv lub hlwb; kev puas tsuaj ntawm kev kawm thiab kev nco), Cov kab mob Parkinson (piv txwv li, qhov tshwm sim los ntawm kev sib sau ntawm -synuclein thiab poob ntawm dopaminergic neurons; tremors thiab nqaij rigidity) thiab amyotrophic lateral sclerosis (xws li, tsub zuj zuj ntawm TAR DNA-binding protein 43; nce degeneration ntawm motorneurons ib lub cev muaj zog; cov leeg tsis muaj zog). yog txhawb los ntawm kev laus [6,62–64].

Nws kuj tau pom tias cov cim kev laus, xws li txo qhov ntev ntawm telomere thiab / organomic instability, epigenetic alterations, mitochondrial dysfunction, cellular senescence, poob ntawm proteostasis, hloov nyob rau hauv cov kev ua ntawm nutrient-sensing pathways thiab intercellular kev sib txuas lus, as well as candle kuaj pom hauv Alzheimer's disease, Parkinson's disease thiab amyotrophic lateral sclerosis.

Txawm li cas los xij, nyob rau hauv amyotrophic lateralsclerosis, qhov txo qis telomere ntev, genomic instability, cellular senescence, thiab kev hloov hauv kev sib txuas lus intercellular tej zaum yuav yog lub ntsiab pab cuam [63,64]. Yog li, nyob rau hauv tshooj no, peb luv luv qhia txog cov cim kev laus tseem ceeb thiab lawv txoj kev sib txuas nrog kev txhim kho ntawm cov hnub nyoog hais txog cov kab mob neurodegenerative saum toj no.

Ntxiv mus, raws li cov ntaub ntawv (xws li, kev tswj hwm thiab kev cuam tshuam ntawm cov tshuaj xenomorphic thiab caloricrestriction) peb nthuav qhia cov kev taw qhia tseem ceeb uas ua rau muaj kev hloov pauv ntawm cov txheej txheem kev laus, tawm tswv yim tias inhibition lossis activation ntawm cov txheej txheem no yuav siv tau rau kev ncua tsis tau tsuas yog kev laus tab sis kuj muaj feem cuam tshuam nrog neurodegenerative. kab mob, txhim kho kev kawm tsis zoo thiab kev nco, nrog rau kev txhawb nqa lub neej.

2.1. Nutrient Sensing Pathways

Kev hloov pauv hauv kev ua ntawm txoj kev paub txog zaub mov yuav muaj lub luag haujlwm hauv kev laus thiab kev loj hlob ntawm cov kab mob uas muaj hnub nyoog. Nws tau raug pom tias kev txwv caloric thiab kev yoo mov tuaj yeem ua rau muaj kev laus, nthuav dav, tsim cov teebmeem neuroprotective, thiab tiv thaiv cov kab mob hnub nyoog los ntawm lub zog (cov khoom noj) sensing insulin/insulin-zoo li growthfactor (IGF) 1 (IIS), AMP (adenosine monophosphate) activated serine-threonineprotein kinase (AMPK), Sirtuin 1 (SIRT1) thiab transcriptional factor FOXOs (Forkhead boxOs) [65–68].

Cov kev tshawb fawb yav dhau los qhia tau hais tias kev txwv caloric tuaj yeem txo IGF, insulin, qabzib, thiab cov amino acid ntau ntxiv, thaum nce NAD + (nicotinamide adenine dinucleotide) thiab AMP qib (Daim duab 1).

Cov kev hloov pauv no tau hnov ​​​​los ntawm (i) IIS txoj hauv kev, qhib los ntawm kev nce IGF thiab qib qabzib; (ii) AMPK, uas hnov ​​​​cov xeev qis zog ntawm qib AMP nce; (iii) SIRT1, uas tseem hnov ​​​​qab lub zog qis ntawm NAD + qib (NAD+-dependent protein deacetylase); thiab (iv) lub hom phiaj ntawm lub hom phiaj ntawm rapamycin (mTOR), uas hnov ​​​​qhov siab amino acid theem ua rau muaj kev ntxhov siab, oxidative metabolism, txhim kho DNA, kev ruaj ntseg ntawm epigenetic thiab nce nyob rau hauv ntev [69–71].Nutrients 2021, 13, {{7 }} ntawm 38Os) [65–68].

Cov kev tshawb fawb yav dhau los qhia tau hais tias kev txwv caloric tuaj yeem txo qis IGF, insulin, qabzib, thiab amino acid qib, thaum nce NAD + (nicotinamide adenine dinucleotide) thiab qib AMP (Daim duab 1).

Cov kev hloov pauv no tau hnov ​​​​los ntawm (i) IIS txoj hauv kev, qhib los ntawm nce IGF thiab qib qabzib; (ii) AMPK, uas hnov ​​​​cov xeev qis zog ntawm qib AMP nce; (iii) SIRT1, uas tseem hnov ​​​​qab lub zog qis ntawm NAD + qib (NAD+-dependent protein deacetylase); thiab (iv) lub hom phiaj ntawm lub hom phiaj ntawm rapamycin (mTOR), uas hnov ​​​​cov amino acid ntau ntau ua rau muaj kev ntxhov siab, oxidative metabolism, txhim kho DNA kho, epigenetic stability thiab ua kom lub neej ntev.

Txo kev ua haujlwm ntawm IIS txoj hauv kev tuaj yeem txuas ntxiv lub neej [72], zoo ib yam li mTORinhibitor rapamycin-evoked nce hauv lifespan [9]. Nws kuj tau pom tias txo qis IIS cov cim qhia txo qis kev sib xyaw ua ke ntawm cov tshuaj lom neeg ntawm A 1-42 (amyloid -peptide 1-42), qhia tias qhov txo qis ntawm cov tshuaj insulin tuaj yeem tiv thaiv kev sib xyaw ntawm cov protein ntau hauv cov kab mob neurodegenerative, xws li Alzheimer'sdisease. [73].

Ntxiv mus, mTOR (ib tug serine / threonine protein kinase) yog lub ntsiab regulator ntawm cellular loj hlob thiab loj tsub zuj zuj, uas muaj mTORC1 thiab mTORC2 complexes [6]. mTORC1 tuaj yeem sib xyaw cov cim los ntawm cov khoom noj khoom haus, kev loj hlob, lub zog, thiab qib oxygen los txhawb kev loj hlob ntawm tes thiab kev loj hlob (piv txwv li, txhim kho lub zog metabolism / glycolysis thiab nucleotide, protein, nrog rau lipid synthesis thiab inhibition ofcatabolism / autophagy) [74,75] ( Daim duab 1).

Tseeb, piv txwv li, mTORC1 txhawb nqa cov proteinsynthesis los ntawm phosphorylation ntawm S6K1 (ribosomal protein S6 kinase 1) thiab 4EBP1 (eukaryotic translation pib qhov tseem ceeb 4E binding protein 1) molecules, uas cov txheej txheem yuav ua tau los ntawm Akt kinase (protein 75 B,) [6] 76] (Daim duab 1).

Ntxiv mus, mTORC1 tuaj yeem cuam tshuam autophagy los ntawm inhibition ntawm ULK1 (Uncoordinated/Unc-51-xws li kinase 1) uas impedes lub cellular homeostasis-tso cov txheej txheem (xws li, muab cov as-ham understarvation thiab tshem tawm cov organelles puas thiab misfolded proteins) [75,77].

Yog li, inhibition ntawm mTORC1 cov teebmeem ntawm autophagy tej zaum yuav yog ib qho cuab yeej tseem ceeb los txo cov txheej txheem ntawm lub hnub nyoog (cov cim kev laus, xws li poob ntawm proteostasis) thiab txhawb kev ua neej ntev [6](Daim duab 1). Nws kuj tau pom tias mTORC2 muaj lub luag haujlwm hauv cytoskeleton reorganization (txuas mus rau kev loj hlob ntawm tes) thiab cell survival modulation [75,78].

For more information:1950477648nn@gmail.com