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求文献两篇，信息如下，谢谢：
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J Cell Mol Med. 2010 Feb 16. [Epub ahead of print]
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Inter-connection between mitochondria and HIFs./ h' X9 d7 L& _ m# m& z' U
Tormos KV, Chandel NS.$ D! L" H5 H+ A1 n' V1 j
+ N0 J( Q5 j" ]# w# e+ cDivision of Pulmonary & Critical Care Medicine, Department of Medicine, Northwestern University Medical School, Chicago, IL 60611.4 Z3 R* Z) s" D/ S& c1 l
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The transcription factors hypoxia inducible factor 1 and 2 (HIF-1 and HIF-2) regulate multiple responses to physiological hypoxia such as transcription of the hormone erythropoietin (EPO) to enhance red blood cell proliferation, vascular endothelial growth factor (VEGF) to promote angiogenesis and glycolytic enzymes to increase glycolysis. Recent studies indicate that HIFs also regulate mitochondrial respiration and mitochondrial oxidative stress. Interestingly, mitochondrial metabolism, respiration and oxidative stress also regulate activation of HIFs. In this review we examine the evidence that mitochondria and HIFs are intimately connected to regulate each other resulting in appropriate responses to hypoxia.
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& ?" f( V5 j9 }- ]PMID: 20158574 [PubMed - as supplied by publisher]/ {0 N" w6 u0 f/ z) T" Q u
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5 R* U A+ `0 Ehttp://www3.interscience.wiley.com/journal/123286409/abstract
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Biochim Biophys Acta. 2010 Feb 11. [Epub ahead of print]$ Q6 G/ v1 r+ ?) k1 e- e
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Hypoxia and mitochondrial oxidative metabolism.& G5 m: I& G8 \; w! |& `- W
Solaini G, Baracca A, Lenaz G, Sgarbi G.4 S; R( J: _9 ]+ M& q; s: u
. ]! V& S, _3 \) E2 x8 p3 }Department of Biochemistry "G. Moruzzi", University of Bologna, Bologna, Italy.
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It is now clear that mitochondrial defects are associated with a large variety of clinical phenotypes. This is the result of the mitochondria's central role in energy production, reactive oxygen species homeostasis, and cell death. These processes are interdependent and may occur under various stressing conditions, among which low oxygen levels (hypoxia) is certainly prominent. Cells exposed to hypoxia respond acutely with endogenous metabolites and proteins promptly regulating metabolic pathways, but if low oxygen levels are prolonged, cells activate adapting mechanisms, the master switch being the hypoxia-inducible factor 1 (HIF-1). Activation of this factor is strictly bound to the mitochondrial function, which in turn is related with the oxygen level. Therefore in hypoxia, mitochondria act as [O(2)] sensors, convey directly or indirectly signals to HIF-1, contribute to the cell redox potential, ion homeostasis, and energy production. Although over the last two decades cellular responses to low oxygen tension have been studied extensively, mechanisms underlying these functions are still indefinite. Here we review current knowledge of the mitochondrial role in hypoxia, focusing mainly on their role in cellular energy and reactive oxygen species homeostasis in relation with HIF-1 stabilization. In addition, we address the involvement of HIF-1 and the inhibitor protein of F(1)F(0)-ATPase in the hypoxia-induced mitochondrial autophagy. Copyright © 2009. Published by Elsevier B.V.
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9 T- N) t" a& Z* a# Y* l: C! o7 NPMID: 20153717 [PubMed - as supplied by publisher]# O4 P- x/ R1 H# \) H$ r
, G6 ]* O" B6 v/ E: d7 i8 qhttp://www.sciencedirect.com/sci ... 8d4952b2857d3d6d7a9 |
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发表于 2010-2-19 20:22
发表于 2010-2-19 20:45
