Adaptation to high altitude hypoxia as a factor preventing development of myocardial ischemic necrosis

Меерсон, Ф. З.; Gomzakov, Oleg A.; Shimkovich, M. V.

doi:10.1016/0002-9149(73)90806-0

Cited by 66 publications

(53 citation statements)

References 5 publications

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“…Many studies showed that intermittent hypoxia might have the cardioprotective effects similar to those observed in ischemic preconditioning [2][3][4][5][6][7][8]. A number of studies have attempted to define the mechanisms of this phenomenon and several potential factors have been proposed to be involved in the protective mechanism afforded by intermittent hypoxia [3,[5][6][7][9][10][11], however, the precise mechanisms underlying the protective effects of intermittent hypoxia on ischemic hearts are far from clear.…”

Section: Introductionmentioning

confidence: 92%

Intermittent hypoxia attenuates ischemia/reperfusion induced apoptosis in cardiac myocytes via regulating Bcl-2/Bax expression

et al. 2003

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Intermittent hypoxia has been shown to provide myocardial protection against ishemia/reperfusion-induced injury. Cardiac myocyte loss through apoptosis has been reported in ischemia/reperfusion injury. Our aim was to investigate whether intermittent hypoxia could attenuate ischemia/reperfusion-induced apoptosis in cardiac myocytes and its potential mechanisms. Adult male Sprague-Dawley rats were exposed to hypoxia simulated 5000 m in a hypobaric chamber for 6 h/day, lasting 42 days. Normoxia group rats were kept under normoxic conditions. Isolated perfused hearts from both groups were subjected to 30 min of global ischemia followed by 60 min reperfusion. Incidence of apoptosis in cardiac myocytes was determined by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) and DNA agarose gel electrophoresis. Expressions of apoptosis related proteins, Bax and Bcl-2, in cytosolic and membrane fraction were detected by Western Blotting. After ischemia/reperfusion, enhanced recovery of cardiac function was observed in intermittent hypoxia hearts compared with normoxia group. Ischemia/ reperfusion-induced apoptosis, as evidenced by TUNEL-positive nuclei and DNA fragmentation, was significantly reduced in intermittent hypoxia group compared with normoxia group. After ischemia/reperfusion, expression of Bax in both cytosolic and membrane fractions was decreased in intermittent hypoxia hearts compared with normoxia group. Although ischemia/reperfusion did not induce changes in the level of Bcl-2 expression in cytosolic fraction between intermittent hypoxia and normoxia groups, the expression of Bcl-2 in membrane fraction was upregulated in intermittent hypoxia group compared with normoxia group. These results indicated that the cardioprotection of intermittent hypoxia against ischemia/reperfusion injury appears to be in part due to reduce myocardial apoptosis. Intermittent hypoxia attenuated ischemia/reperfusion-induced apoptosis via increasing the ratio of Bcl-2/Bax, especially in membrane fraction.

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Section: Introductionmentioning

confidence: 92%

Intermittent hypoxia attenuates ischemia/reperfusion induced apoptosis in cardiac myocytes via regulating Bcl-2/Bax expression

et al. 2003

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“…Similar to sublethal ischemia, hypoxia elicits PC-like response in which the myocardium develops an adaptive phenotype leading to resistance against subsequent lethal I/R injuries (Meerson et al, 1973;Bolli, 2000;Xi et al, 2002). This cardioprotection seems to be essentially mediated by hypoxia-inducible factor 1␣ (HIF-1␣) (Cai et al, 2003).…”

Section: Mirnas In Hypoxic Preconditioningmentioning

confidence: 99%

MicroRNAs: New Players in Cardiac Injury and Protection

Kukreja¹,

Yin²,

Salloum³

2011

Mol Pharmacol

122

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MicroRNAs (miRNAs) have emerged as a novel class of endogenous, small, noncoding RNAs that negatively regulate gene expression via degradation or translational inhibition of their target mRNAs. Over 700 miRNAs have been identified and sequenced in humans, and the number of miRNA genes is estimated at more than 1000. Individual miRNA is functionally important as a transcription factor because it has the ability to regulate the expression of multiple genes through binding to its target with imperfect or perfect complement. In the heart, miRNAs have been involved in several clinical scenarios, such as ischemia/reperfusion (I/R) injury and heart failure suggesting that regulation of their function could be used as a novel cardioprotective strategy. In particular, miRNA-1, miRNA-21, miRNA-24, miRNA-29, miRNA-92a, miRNA-126, miRNA-133, miRNA-320, miRNA-199a, miRNA-208, and miRNA-195 have been shown to be regulated after I/R injury. Because tissue miRNAs can be released into circulating blood, they also offer exciting new opportunities for developing sensitive biomarkers, including miRNA-1, miRNA-126, miR-208, and miRNA-499, for acute myocardial infarction and other cardiac diseases.

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“…This is exemplified by hypoxic preconditioning (Sharp et al, 2004), in which previous exposure to hypoxia leads to neuroprotection from subsequent hypoxic exposure. Other highly aerobic tissues, such as the heart, adapt to hypoxia by mechanisms that include increased mitochondrial mass and therefore respiratory capacity (Ou and Tenney, 1970;Meerson et al, 1972Meerson et al, , 1973Eells et al, 2000). Such data suggest that augmentation of bioenergetic capacity through mitochondrial biogenesis, the generation of new mitochondria, could improve the ability of certain cells to survive a hypoxic stress.…”

Section: Introductionmentioning

confidence: 99%

Transient Hypoxia Stimulates Mitochondrial Biogenesis in Brain Subcortex by a Neuronal Nitric Oxide Synthase-Dependent Mechanism

Gutsaeva¹,

Carraway²,

Suliman³

et al. 2008

J. Neurosci.

168

112

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The adaptive mechanisms that protect brain metabolism during and after hypoxia, for instance, during hypoxic preconditioning, are coordinated in part by nitric oxide (NO). We tested the hypothesis that acute transient hypoxia stimulates NO synthase (NOS)-activated mechanisms of mitochondrial biogenesis in the hypoxia-sensitive subcortex of wild-type (Wt) and neuronal NOS (nNOS) and endothelial NOS (eNOS)-deficient mice. Mice were exposed to hypobaric hypoxia for 6 h, and changes in immediate hypoxic transcriptional regulation of mitochondrial biogenesis was assessed in relation to mitochondrial DNA (mtDNA) content and mitochondrial density. There were no differences in cerebral blood flow or hippocampal PO 2 responses to acute hypoxia among these strains of mice. In Wt mice, hypoxia increased mRNA levels for peroxisome proliferator-activated receptor-␥ coactivator-1␣ (PGC-1 ␣), nuclear respiratory factor-1, and mitochondrial transcription factor A. After 24 h, new mitochondria, localized in reporter mice expressing mitochondrial green fluorescence protein, were seen primarily in hippocampal neurons. eNOS Ϫ/Ϫ mice displayed lower basal levels but maintained hypoxic induction of these transcripts. In contrast, nuclear transcriptional regulation of mitochondrial biogenesis in nNOS Ϫ/Ϫ mice was normal at baseline but did not respond to hypoxia. After hypoxia, subcortical mtDNA content increased in Wt and eNOS Ϫ/Ϫ mice but not in nNOS Ϫ/Ϫ mice. Hypoxia stimulated PGC-1␣ protein expression and phosphorylation of protein kinase A and cAMP response element binding (CREB) protein in Wt mice, but CREB only was activated in eNOS Ϫ/Ϫ mice and not in nNOS Ϫ/Ϫ mice. These findings demonstrate that hypoxic preconditioning elicits subcortical mitochondrial biogenesis by a novel mechanism that requires nNOS regulation of PGC-1␣ and CREB.

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Adaptation to high altitude hypoxia as a factor preventing development of myocardial ischemic necrosis

Cited by 66 publications

References 5 publications

Intermittent hypoxia attenuates ischemia/reperfusion induced apoptosis in cardiac myocytes via regulating Bcl-2/Bax expression

Intermittent hypoxia attenuates ischemia/reperfusion induced apoptosis in cardiac myocytes via regulating Bcl-2/Bax expression

MicroRNAs: New Players in Cardiac Injury and Protection

Transient Hypoxia Stimulates Mitochondrial Biogenesis in Brain Subcortex by a Neuronal Nitric Oxide Synthase-Dependent Mechanism

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