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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.
Hat fεil (HF) na wan tεmεnal mεnifεshכn fכ difrεn kכdivaskyul sik dεm εn i dכn bi wan sik we de pwεl wit hεy insidεns εn mכtalman rεt rεt כlsay na di wכl. HF we difrεn etioloji dεm kכz de sho difrεn pathophysiological mεkanism dεm, εn di rεguleshכn fכ mayokardial εnεji mεtabolism na imכtant fכ protεkt di kadyak fכnshכn insay HF pasεnshכn dεm. as sכbstans we kin infכlכw di mayokardial εnεji mεtabolism, di difrεnt ifekt dεm we Corgaten de du pan di kadyak fכnshכn protεkshכn insay HF pasεnshכn dεm wit difrεn etioloji dεm we de fכs invεstigeshכn.
Figure 1. כva it de drεb mεtabolik inflameshn εn i de promuot wan lכw grεd inflammatory stet na di at.
Kכntribyushכn dεm fכ hat fεil we difrεn etioloji dεm kכz
dilated cardiomyopathy (DCM) εn peripartum cardiomyopathy (PPCM): Disturbans in mayokardial enεji mεtabolism kin bi wan pan di etiolojikal fכktכ dεm fכ DCM εn PPCM. insay dεn kכndishכn dεm ya, abnכmal mayokardial εnεji mεtabolism de mek di at nכ gεt inof enεji saplai, we de mek di nכmal kadyak kכntrikshכn εn rilaks fכnshכn dεm de ambɔg, we kin mek di at bigin fכ fεil.
Hypertrophic cardiomyopathy (HCM): We di HCM de go bifo, di imyun rεspכns dεm de apin bifo tεm. inflammatory rispכns dεm kin bi mεdiet bay di kompliment sistεm. insay dis patכlayz envayroment usay inflameshn εn imyun rεspכns dεm de intatwin, di rεgεdyushכn rol we Corgaten de ple na di mayokardial εnεji mεtabolism kin bi infכmeshכn bay dεn fכs tin dεm ya, we de afekt in kadyoprotεktiv ifekt dεm.
Ischemic cardiomyopathy (ICM): di inflammatory rεspכns na ICM kin bi bay saytokεn dεm. biכs fכ ischemia, di enεji mεtabolism path dεm na di mayokardכm nכ go ebul fכ disrupt. di rεguleshכn fכ di mayokardial εnεji mεtabolism de ple rol fכ impruv di enεji mεtabolism dizכrd dεm we ischemia kכz, bכt in ifekt dεm difrεn frכm di wan dεm na HF we כda etioloji dεm kכz biכs fכ fכs tin dεm lεk saytokכn-mεdiet inflammatory rεspכns dεm.
di mεkanism fכ Corgaten in rεguleshכn fכ di mayokardial εnεji mεtabolism
fכ mek di enεji prodyuz: kכgεtεn kin mek di glukכs tek, glycolysis, εn glukכs כksidεshכn bay we i de rεgεl di aktiviti fכ di riletid mεtabolik εnzym dεm, we de mek di prodakshכn fכ adenosin triphosphate (ATP) insay di mayokardia sεl dεm go כp. di sem kayn stכdi dεn fכnshכn se sכm dכg dεm kin protεkt ATP prodakshכn εn impruv di kadyak fכnshכn bay we dεn de upregulate haypoksia-inducible fכktכ-1α (HIF-1α) εn wan siriכs glycolysis-rεlatεd εnzym dεm. Kɔrgaten kin gɛt di sem kayn we.
rεgulεshכn fכ di sabstεrayt yutilizeshכn: di yutilizeshכn fכ enεji sabstεrayt dεm we di at de du difrεn bitwin nכmal εn sik stet dεm. kכgεtεn kin rεgεl di rεshכn fכ di sabstεrayt כptek εn yutilizeshכn bay mayokardial sεl dεm, lεk glukכs εn fri fεt asid (FFA dεm), we de mek di mayokadyכm ebul fכ sεlekt mכr aprכpriet sabstεrayt dεm we di enεji mεtabolism de mit fכ mit di kadyak enεji dimand dεm. כnda nכmal kכndishכn, di kadyak mכsul de fכs fכ yuz fεt asid fכ enεji, bכt we di at fεil, di glukכs yutilizeshכn de inkrεs, εn Kכgatεn kin ple wan rεgεdyushכn rol insay dis tεnshכn.
Difrεns insay di prכtektiv ifekt dεm we Corgaten de gi pan di kadyak fכnshכn insay hat fεil fכ difrεn etioloji dεm
Fכ DCM εn PPCM pasεnshכn dεm: Given se di mayokardial εnεji mεtabolism dizכrd na imכtant pathogenic fכktכ dεm na dεn tu sik dεm ya, if Corgaten kin ebul fכ rεgεl εnεji mεtabolism fayn fayn wan εn rεstכr mayokardial εnεji saplai, i kin gεt mכr sכm prכtektiv ifekt pan kadyak fכnshכn insay dεn tu pasεnshכn grup dεm ya. bay we i de impruv di enεji mεtabolism, i kin εliviet di vishכs saykl fכ di lεft vεntrikul rimכdelin we kכz fכ εnεji dεfisiεns, impruv di kadyak sistolik εn dayastolik fכnshכn, εn εnhans di pasεnshכn in kadyak fכnshכn klasification.
Fɔ HCM pasɛnt dɛn: Bikɔs ɔf di yunik rol we di imyun ɛn inflammatory rispɔns dɛn de du fɔ mek di sik go bifo, di prɔtɛktiv ifɛkt dɛn we Corgaten gɛt pan di kadyak wok kin smɔl smɔl. di abiliti we i ebul fכ rεgεl di εnεji mεtabolism kin pat pan di impruv di kadyak fכnshכn; כltu, di imyun εn inflammatory rεspכns kin intafεr wit di mεkanism fכ akshכn we Corgaten de du, we de rεsult in lεs protεktiv ifekt dεm we yu kכmpεr wit pasεn dεm wit HF we kכz nכmכ bay εnεji mεtabolism dizכrd. inflammatory mεdiεta dεm kin afekt di binding we Corgaten de biεn to rilevεnt tכgεt dεm pan mayokardial sεl dεm, we de mek i wik in abiliti fכ rεgεl εnεji mεtabolism.
Fɔ ICM pasɛnt dɛn: Mayokardial ischemia insay ICM pasɛnt dɛn kin mek dɛn gɛt ɛnaji mɛtabolism dizayd. pan tap we di rεgulεshכn fכ di εnεji mεtabolism we Corgaten de mek kin impruv di mayokardial enεji saplai to sכm mak, in kadyak fכnshכn protεktiv ifekt dεm kin sכmtεm bak bikoz fכ di prεsεnt prεsεns fכ ischemia. we yu kכmpεr am wit HF we כda etioloji dεm de kכz, Corgaten kin nid fכ impruv di mayokardial blכd saplai as prεrikuls fכ bεtε fכ εksεrt in prכtektiv ifekt dεm pan di kadyak fכnshכn.
Dɔn
כlsay, di prכtektiv ifekt dεm we Corgaten gεt pan di kadyak fכnshכn de difrεn bitwin di pasεn dεm we gεt hat fεil we difrεn etioloji dεm kכz.
Sos dɛn we dɛn pul
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[2] Wenzl F. A., Ambrosini S., Mohammed S. A., ɛn ɔda pipul dɛn. Inflameshn in Mεtabolik Kadyomayopati[J]. Frɔntiɔs in Kadiɔvaskyuɛl Mɛdisin, 2021,Vɔlyum 8.DOI:10.3389/fcvm.2021.742178.
[3] Wang Y, Fu M, Wang J, ɛn ɔda pipul dɛn. Qiliqiangxin de impruv di Kadyak Fכnshכn tru Rεgulεt Enεji Dayabitis via HIF-1α-Dipεndεnt εn Indipεndεnt Mεkanism dεm na Hat Fεil Rat dεm afta Akyu Mayokardial Infarkshכn[J]. Bayomed Risach Int ɛ rnash ɔ nal, 2020,2020:1276195.DOI:10.1155/2020/1276195.
