Adenine nucleotide translocase 1 overexpression protects cardiomyocytes against hypoxia via increased ERK1/2 and AKT activation
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- 作者：Julia Wintera ; b ; 1 ; Inga Klumpea ; c ; 1 ; Jacqueline Hegerd ; Ursula Raucha ; Heinz-Peter Schultheissa ; Ulf Landmessera ; Andrea Dö ; rnera ; andrea.doerner@charite.de" class="auth_mail" title="E-mail the corresponding author
- 关键词：ANT1 ; adenine nucleotide translocase 1 ; ANT1-TG ; ANT1-transgenic ; ERK1/2 ; extracellular signal-regulated kinases 1 and 2 ; AKT ; protein kinase B ; WT ; wild type ; HIF-1α ; hypoxia-inducible factor 1α ; LDH ; lactate dehydrogenase ; CAT ; carboxyatractyloside ; MPTP ; mitochondrial permeability transition pore ; Δψm ; mitochondrial inner membrane potential
- 刊名：Cellular Signalling
- 出版年：2016
- 出版时间：January 2016
- 年：2016
- 卷：28
- 期：1
- 页码：152-159
- 全文大小：925 K
文摘
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ANT1 overexpression stabilizes the mitochondrial membrane potential in hypoxic cardiomyocytes.
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ANT1 overexpression increases activation of ERK1/2 and AKT under hypoxia.
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ANT1 overexpression increases HIF-1α and induction of the anaerobic pathway, stabilizing the intracellular ATP content.
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Inhibition of ERK1/2, AKT phosphorylation, or ANT activity eliminates cell protection in ANT1-transgenic cardiomyocytes.
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ANT1 is part of a signalling network that includes ERK1/2 and AKT activation and results in cell survival.