Human adaptation to ischemia by preconditioning or unstable angina: involvement of nuclear factor kappa B, but not hypoxia-inducible factor 1 alpha in the heart

Czibik, Gabor; Wu, Zhongkai; Berne, Gabrielle Paulsson; Tarkka, Matti; Vaage, Jarle; Laurikka, Jari; Järvinen, Otso; Valen, Guro

doi:10.1016/j.ejcts.2008.07.066

Cited by 17 publications

(4 citation statements)

References 25 publications

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“…According to the results of the study by Kawata et al, HIF-1α does not involve in VEGF upregulation in ischemic preconditioning pathway [37] . Furthermore, NF-κB regulated genes were influenced by ischemic preconditioning but hypoxia inducible genes were not in the patients with angina, undergoing coronary artery bypass grafting [38] . Ischemic postconditioning is a cardioprotective modality against reperfusion injury through series of brief reflow interruptions applied at the very onset of reperfusion [39] .…”

Section: Involvement Of Hif-1 In Ischemic Preconditioning and Post Comentioning

confidence: 99%

Hypoxia inducible factor 1 (HIF-1) and cardioprotection

2010

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Since its discovery in early 1990s, hypoxia inducible factor 1 (HIF-1) has been increasingly recognized for its key role in transcriptional control of more than a hundred genes that regulate a wide-spectrum of cellular functional events, including angiogenesis, vasomotor control, glucose and energy metabolism, erythropoiesis, iron homeostasis, pH regulation, cell proliferation and viability. Evidence accumulated during the past 7 years suggests a critical role for HIF-1α in mediating cardioprotection. The purpose of our present article is to provide an updated overview on this important regulator of gene expression in the cellular stress-responsive and adaptive process. We have particularly emphasized the involvement of HIF-1 in the induction of cardioprotective molecules, such as inducible nitric oxide synthase (iNOS), hemeoxygenase 1 (HO-1), and erythropoietin (EPO), which in turn alleviate myocardial damages caused by harmful events such as ischemia-reperfusion injury. Despite these advances, further in-depth studies are needed to elucidate the possible coordination or interaction between HIF-1α and other key transcription factors in regulating protein expression that leads to cardioprotection.

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Section: Involvement Of Hif-1 In Ischemic Preconditioning and Post Comentioning

confidence: 99%

Hypoxia inducible factor 1 (HIF-1) and cardioprotection

2010

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“…Several cycles of ischemia followed by short episodes of reperfusion signifi cantly reduced the infarct size after a subsequent myocardial ischemia. Very recent studies with patients suffering from cardiac angina corroborate these experimental data, that injury-induced ischemic events protect these patients from severe myocardial infarction [ 91 ]. Ischemic preconditioning is not confi ned to the heart.…”

Section: Tissue Protection By Hypoxic Preconditioningmentioning

confidence: 69%

Cellular and Molecular Defenses Against Hypoxia

Frede

Fandrey

2013

High Altitude

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The ability to cope with hypoxia is essential for the development and survival of all vertebrate species. Cellular hypoxia occurs when oxygen demand exceeds oxygen supply. The development of cellular hypoxia depends both on the type of tissue and partial pressure oxygen (PO 2 ) in the tissue, because cells can vary extremely in their physiologic oxygen demand. Under normal conditions up to 90 % of the available oxygen is consumed by mitochondria to yield ATP through oxidative phosphorylation. Thus, oxygen deprivation will always lead to fundamental changes in cell metabolism and function. Different physiological systems have evolved for adaptation to conditions of low oxygen. Acute adaptation includes increased ventilation, changes in metabolism, protection against hypoxia-induced cell death and vasodilation. Adaptations to chronic hypoxia are characterized by the aim to restore oxygen delivery to the tissue. This is achieved by improving the oxygen transport capacity by increasing haemoglobin and red blood cell mass. Furthermore, long-term adaptation includes the remodelling of existing vessels as well as the formation of new vessels to increase blood and concurrently oxygen supply. Most of the hypoxic adaptations implicate gene expression driven by transcription factors especially activated under hypoxic conditions, such as H ypoxia-i nducible f actor 1 (HIF-1). HIF-1 is the best characterized regulators of cellular responses to hypoxia and products of its target genes are involved in all phases of hypoxic adaptation. In addition, for certain tissues a variety of HIF-1 independent molecular changes contributing to the cellular hypoxic response have been described including activation of NF-κB, CREB, and Notch. Particular attention is devoted to a potential cross talk between the oxygen-dependent HIF-1 regulators prolyl-hydroxylase (PHDs) and these HIF-1 independent hypoxia regulated factors which are known to be critical for survival under general stress conditions.

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“…NF-κB exerts a critical effect on regulating cardiomyocyte apoptosis, especially in response to oxidative stress following myocardial infarction (Imam et al, 2018). In human, Czibik et al (2008) reported that NF-κB nuclear translocation was reduced at reperfusion in stable angina patients after ischemic precondition. However, researchers have not conclusively determined whether it exerts cardioprotective effects or deleterious effects.…”

Section: Nuclear Factor-κbmentioning

confidence: 99%

Transcription Factors Involved in the Development and Prognosis of Cardiac Remodeling

Hong

Zhang

2022

Front. Pharmacol.

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To compensate increasing workload, heart must work harder with structural changes, indicated by increasing size and changing shape, causing cardiac remodeling. However, pathological and unlimited compensated cardiac remodeling will ultimately lead to decompensation and heart failure. In the past decade, numerous studies have explored many signaling pathways involved in cardiac remodeling, but the complete mechanism of cardiac remodeling is still unrecognized, which hinders effective treatment and drug development. As gene transcriptional regulators, transcription factors control multiple cellular activities and play a critical role in cardiac remodeling. This review summarizes the regulation of fetal gene reprogramming, energy metabolism, apoptosis, autophagy in cardiomyocytes and myofibroblast activation of cardiac fibroblasts by transcription factors, with an emphasis on their potential roles in the development and prognosis of cardiac remodeling.

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Human adaptation to ischemia by preconditioning or unstable angina: involvement of nuclear factor kappa B, but not hypoxia-inducible factor 1 alpha in the heart

Abstract: Cardiac function was improved by ischemic preconditioning in both stable and unstable patients. Unstable angina per se had no effect. NFkappaB-regulated genes were influenced by ischemic preconditioning, but hypoxia-inducible genes were not.

Cited by 17 publications

References 25 publications

Hypoxia inducible factor 1 (HIF-1) and cardioprotection

Hypoxia inducible factor 1 (HIF-1) and cardioprotection

Cellular and Molecular Defenses Against Hypoxia

Transcription Factors Involved in the Development and Prognosis of Cardiac Remodeling

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