Chronic intermittent hybobaric hypoxia protects against cerebral ischemia via modulation of mitoKATP

Zhang, Shixiao; Guo, Zan; Yang, Shijie; Ma, Huijuan; Fu, Congrui; Wang, Sheng; Zhang, Yi; Liu, Yixian; Hu, Jie

doi:10.1016/j.neulet.2016.10.025

Cited by 14 publications

(9 citation statements)

References 26 publications

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“…Thus, higher density of mKATP channel distribution in brain results in slight depolarization, which was observed in the literature and in our studies [63,64], while lower amount of the channels in the heart and liver was of no effect on ΔΨ m even at full activation [24,65,66]. Elevated expression of mKATP channel and the channel activation that were observed under hypoxia [20,21,41,59] increase the "weight" of ATP-sensitive K + transport in the regulation of mitochondrial functions and metabolism. This is still more visible in malignant cells functioning in hypoxic environment, in which overexpression of mKATP channel was shown [53].…”

Section: Direct Bioenergetic Consequences Of Mkatp Channels Openingsupporting

confidence: 73%

“…As it was reported, different regimens of hypoxia exposure (such as intermittent hypobaric hypoxia [10,21,41], brief hypoxia exposure (hypoxic preconditioning) [25], chronic hypoxia [20,27,59]) resulted in the activation of potassium transport: mKATP channel [10,20,21,41], BK Ca channel [27] and K + /H + exchange [21]. According to these data, mitochondrial K + channel opening and activation are ubiquitous consequence of oxygen shortage, indicating that K + channel opening is involved in the response of mitochondria to the lack of oxygen.…”

Section: Mitochondrial Potassium Transport Under Oxygen Deficiencymentioning

confidence: 99%

“…The impact of ATPsensitive K + transport on the oxygen consumption, membrane potential, ATP synthesis, Ca 2+ transport and ROS production is largely dependent on the abundance of the channel in mitochondrial membrane. Oxygen deficiency affects functional consequences of mKATP channels opening by modulating channels expression and activity [20,53,59]. As it was shown in cardiomyocytes, the activation of cardiac mKATP channels under hypoxia was mediated by the interactions of conducting subunit Kir6.2 with heat shock protein 90, HSP90 [25] and Kir6.1 with gap junction protein connexin 43 and PKCε [26].…”

Section: Mitochondrial Potassium Transport Under Oxygen Deficiencymentioning

confidence: 99%

“…Thus, under oxygen deprivation, mKATP channel activation reduced mitochondrial Ca 2+ loading [57,79], preserved ATP levels [67,77] and increased cell survival [16,40,41,80] by suppression of apoptosis via targeting glycogen synthase kinase 3β (GSK3β), an enzyme involved in triggering cell death by promotion of the opening of mitochondrial permeability transition pore, mPTP [81]. Suppression of cell death pathways resulted in stabilization of membrane potential [16,59,80] and the restoration of ATP synthesis [82]. Increased expression of both Kir6.2 [59] and SUR2A [37], similar to pharmacological mKATP channels opening, too was shown to improve the viability and the resistance of cardiomyocytes to hypoxia.…”

Section: Functional Consequences and Molecular Targets Of Mkatp Channmentioning

confidence: 99%

“…Suppression of cell death pathways resulted in stabilization of membrane potential [16,59,80] and the restoration of ATP synthesis [82]. Increased expression of both Kir6.2 [59] and SUR2A [37], similar to pharmacological mKATP channels opening, too was shown to improve the viability and the resistance of cardiomyocytes to hypoxia.…”

Section: Functional Consequences and Molecular Targets Of Mkatp Channmentioning

confidence: 99%

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Mitochondrial KATP Channel Function under Hypoxia

Акопова¹

2018

Hypoxia and Anoxia

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Hypoxic states and conditions result in complex alterations of the energetics and metabolism at the level of the whole cell and mitochondria, including the modulation of metabolic pathways and activation of transcription factors and signaling events. Common feature of the alterations of mitochondrial functions under hypoxia is the activation of mitochondrial potassium channels. Most studied of mitochondrial potassium channels, ATP-sensitive K + channel (mKATP channel), is supposed to play important role in the adaptation to hypoxia. However, the main obstacles in the understanding of mKATP channel functions under hypoxic conditions are contradictory data on the direct bioenergetic effects of mKATP channels opening and the lack of knowledge on cell specificity of mKATP channel functioning and of cell signaling pathways triggered by mKATP channels opening. So, the aim of this review was to outline the present knowledge on mKATP channel functions under hypoxia and to discuss how alterations to mitochondrial energetics and metabolism caused by mKATP channels opening (primarily at the level of ROS production and ATP synthesis) could be involved in multiple adaptive responses of a living organism to oxygen deprivation conditions.

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Section: Direct Bioenergetic Consequences Of Mkatp Channels Openingsupporting

confidence: 73%

Section: Mitochondrial Potassium Transport Under Oxygen Deficiencymentioning

confidence: 99%

Section: Mitochondrial Potassium Transport Under Oxygen Deficiencymentioning

confidence: 99%

Section: Functional Consequences and Molecular Targets Of Mkatp Channmentioning

confidence: 99%

Section: Functional Consequences and Molecular Targets Of Mkatp Channmentioning

confidence: 99%

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Mitochondrial KATP Channel Function under Hypoxia

Акопова¹

2018

Hypoxia and Anoxia

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The effect of chronic intermittent hypobaric hypoxia improving liver damage in metabolic syndrome rats through ferritinophagy

Cui,

Mi,

Wang

et al. 2023

Pflugers Arch - Eur J Physiol

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Background and aimStudies have con rmed that hepatic iron overload is one of the important factors causing liver damage in metabolic syndrome (MS). As a special form of autophagy, ferritinophagy is involved in the regulation of iron metabolism. Our previous studies have shown that chronic intermittent hypobaric hypoxia (CIHH) can improve the iron metabolism disorder. The aim of this study was to investigate how CIHH improves liver damage through ferritinophagy in rats with MS. MethodsMale Sprague-Dawley rats aged 8-10 weeks were randomly divided into four groups: control (CON), CIHH (exposed to hypoxia at simulated altitude of 5000 meters for 28 days, 6 hours daily), MS model (induced by 16-week high fat diet and 10% fructose water feeding) and MS + CIHH (exposed to CIHH after 16-week MS inducement) groups. Liver index, liver function, iron content, tissue morphology, ferritinophagy, ferroptosis and iron metabolism related protein expression were measured, and the ferritinophagy ux in liver was further analyzed. ResultsCompared with CON rats, MS rats had increased liver index, damaged liver tissue morphology and function, increased total iron and free iron content, disrupted iron metabolism, signi cantly increased oxidative stress indicators in the liver, signi cantly increased expression of ferroptosis-related proteins, reduced expression of nuclear receptor coactivator 4 (NCOA4) and ferritinophagy ux. After CIHH treatment, the degree of liver damage and various abnormal indicators in MS rats were signi cantly improved. ConclusionsCIHH may improve liver damage by promoting NCOA4-mediated ferritinophagy, reducing iron overload, and alleviating ferroptosis in MS rats.

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The Cannabinoid Receptor Agonist WIN55,212-2 Ameliorates Hippocampal Neuronal Damage After Chronic Cerebral Hypoperfusion Possibly Through Inhibiting Oxidative Stress and ASK1-p38 Signaling

Wang¹,

Lin

et al. 2019

Neurotox Res

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Chronic intermittent hybobaric hypoxia protects against cerebral ischemia via modulation of mitoKATP

Cited by 14 publications

References 26 publications

Mitochondrial KATP Channel Function under Hypoxia

Mitochondrial KATP Channel Function under Hypoxia

The effect of chronic intermittent hypobaric hypoxia improving liver damage in metabolic syndrome rats through ferritinophagy

The Cannabinoid Receptor Agonist WIN55,212-2 Ameliorates Hippocampal Neuronal Damage After Chronic Cerebral Hypoperfusion Possibly Through Inhibiting Oxidative Stress and ASK1-p38 Signaling

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