Cardioplegia and Diazoxide Modulate STAT3 Activation and DNA Binding

Hsieh, Yng-Ju; Wakiyama, Hidetaka; Levitsky, Sidney; McCully, James D.

doi:10.1016/j.athoracsur.2007.05.014

Cited by 11 publications

(9 citation statements)

References 23 publications

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“…The potassium channel opener pinacidil was also able to uncouple mitochondria (44). In addition, diazoxide can directly affect phosphorylation events within the cell and ATP synthase activity (46). Hence, pharmacological preconditioning by potassium channel openers has been proposed to reflect partial inhibition of the respiratory chain or uncoupling of mitochondria (47, 48).…”

Section: Pharmacology Of Mitochondrial Potassium Channels: Dark Side mentioning

confidence: 99%

Mitochondrial potassium channels

Szewczyk

Jarmuszkiewicz

Kunz³

2009

IUBMB Life

162

114

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SummaryMitochondrial potassium channels are believed to contribute to cytoprotection of injured cardiac and neuronal tissues. The following potassium channels have been described in the inner mitochondrial membrane: the ATP-regulated potassium channel, the large conductance Ca 21 -activated potassium channel, the voltage-gated Kv1.3 potassium channel, and the twin-pore domain TASK-3 potassium channel. The putative functional roles of these channels include changes in mitochondrial matrix volume, mitochondrial respiration, and membrane potential. In addition, the activity of these channels modulates the generation of reactive oxygen species by mitochondria. In this article, we discuss recent observations on three fundamental issues concerning mitochondrial potassium channels: (i) their molecular identity, (ii) their interaction with potassium channel openers and inhibitors, and (iii) their functional properties.

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Section: Pharmacology Of Mitochondrial Potassium Channels: Dark Side mentioning

confidence: 99%

Mitochondrial potassium channels

Szewczyk

Jarmuszkiewicz

Kunz³

2009

IUBMB Life

162

114

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“…In addition, numerous carcinogens (e.g. nicotine in cigarette smoke [34], diesel exhaust particles [72], hepatitis C virus core protein [73], lipopolysaccharide (LPS) [74]), environmental stress (e.g., ultraviolet light [75], osmotic shock [76], heat shock [77] and oxidative stress [78]) and other factors such as EBV oncoprotein LMP1 [79], HIV-1 Nef protein [80], leptin [81], Ca 2 + /calmodulin-dependent protein kinase IIγ (CaMKIIγ) [82], bile acids and low pH [83], black soy peptides [84], diazoxide [85], isoliquiritigenin [86], and olanzapine [87] have been identified to activate STAT3 (Fig. 1).…”

Section: Stat3 Activation By Diverse Agentsmentioning

confidence: 99%

Targeting the STAT3 signaling pathway in cancer: Role of synthetic and natural inhibitors

Siveen

Sikka

Surana

et al. 2014

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

479

510

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Signal transducers and activators of transcription (STATs) comprise a family of cytoplasmic transcription factors that mediate intracellular signaling that is usually generated at cell surface receptors and thereby transmit it to the nucleus. Numerous studies have demonstrated constitutive activation of STAT3 in a wide variety of human tumors, including hematological malignancies (leukemias, lymphomas, and multiple myeloma) as well as diverse solid tumors (such as head and neck, breast, lung, gastric, hepatocellular, colorectal and prostate cancers). There is strong evidence to suggest that aberrant STAT3 signaling promotes initiation and progression of human cancers by either inhibiting apoptosis or inducing cell proliferation, angiogenesis, invasion, and metastasis. Suppression of STAT3 activation results in the induction of apoptosis in tumor cells, and accordingly its pharmacological modulation by tyrosine kinase inhibitors, antisense oligonucleotides, decoy nucleotides, dominant negative proteins, RNA interference and chemopreventive agents have been employed to suppress the proliferation of various human cancer cells in culture and tumorigenicity in vivo. However, the identification and development of novel drugs that can target deregulated STAT3 activation effectively remains an important scientific and clinical challenge. This review presents the evidence for critical roles of STAT3 in oncogenesis and discusses the potential for development of novel cancer therapies based on mechanistic understanding of STAT3 signaling cascade.

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“…Ischemic heart disease is one of the leading causes of global morbidity and mortality (1). Mitochondrial damage is the principal pathogenesis of myocardial ischemia-reperfusion injury leading to cardiomyocyte death and contractile failure (2, 3, 4, 5, 6, 7) .…”

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confidence: 99%