https://transhumanist.ru/index.php?action=history&feed=atom&title=ACO2 2026-08-10T14:47:03Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=ACO2&diff=4148&oldid=prev 2021-04-29T19:03:06Z

<p>Новая страница: «Aconitate hydratase, mitochondrial precursor (EC 4.2.1.3) (Aconitase) (Citrate hydro-lyase) ==Publications== {{medline-entry |title=Thioredoxin protects mitocho...»</p> <p><b>Новая страница</b></p><div>Aconitate hydratase, mitochondrial precursor (EC 4.2.1.3) (Aconitase) (Citrate hydro-lyase)<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Thioredoxin protects mitochondrial structure, function and biogenesis in myocardial ischemia-reperfusion via redox-dependent activation of AKT-CREB- PGC1α pathway in aged mice.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/33049718<br /> |abstract=Aging is an independent risk factor for cardiovascular diseases, such as myocardial infarction due to ischemia-reperfusion injury (I/R) of the heart. Cytosolic thioredoxin (Trx) is a multifunctional redox protein which has antioxidant and protein disulfide reducing properties. We hypothesized that high levels of Trx will protect against multifactorial disease such as myocardial infarction due to I/R injury in aged mice. Aged mice overexpressing human Trx ([i]Trx-Tg[/i]), mice expressing redox-inactive mutant of human Trx ([i]dnTrx-Tg[/i]) and non-transgenic litter-mates ([i]NT)[/i] were subjected to I/R (60/30 min), and cardiac function, mitochondrial structure and function, and biogenesis involving PGC1α pathway were evaluated in these mice. While aged [i]Trx-Tg[/i] mice were protected from I/R-induced reduction in ejection fraction (EF) and fractional shortening (FS), had smaller infarct with decreased apoptosis and preserved mitochondrial function, aged [i]dnTrx-Tg[/i] mice showed enhanced myocardial injury and mitochondrial dysfunction. Further, [i]Trx-Tg[/i] mice were protected from I/R induced loss of PGC1α, [[ACO2]], [[MFN1]] and [[MFN2]] in the myocardium. The [i]dnTrx-Tg[/i] mice were highly sensitive to I/R induced apoptosis. Overall, our study demonstrated that the loss of Trx redox balance in I/R in aged [i]NT[/i] or [i]dnTrx-Tg[/i] mice resulted in decreased PGC1α expression that decreased mitochondrial gene expression with increased myocardial apoptosis. High levels of Trx, but not mitochondrial thioredoxin (Trx-2) maintained Trx redox balance in I/R resulting in increased PGC1α expression via AKT/CREB activation upregulating mitochondrial gene expression and protection against I/R injury.<br /> <br /> |keywords=* aging<br /> * heart<br /> * ischemia-reperfusion<br /> * mitochondria<br /> * thioredoxin<br /> |full-text-url=https://sci-hub.do/10.18632/aging.104071<br /> }}</div>

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