Liver HIF-1 Alpha Induction Precedes Apoptosis Following Normothermic Ischemia-Reperfusion in Rats

Cursio, Raffaele; Miele, Claudia; Filippa, Nathalie; Obberghen, E. Van; Gugenheim, Jean

doi:10.1016/j.transproceed.2008.05.037

Cited by 33 publications

(35 citation statements)

References 15 publications

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“…Th is pattern is consistent with HIF expression at the border of renal infarct zones only, indicating that dying cells within the critically ischemic region are incapable of mounting a hypoxia adaptive response [25]. We also found that HIF-α isoforms are stabilized in acute hypoxic stress, predominantly in the cortex in rhabdomyolysis-induced kidney injury [26], in the outer stripe of the outer medulla following ischemia and reperfusion [27,28], or in the inner stripe and inner medulla following the induction of distal tubular hypoxic injury by radiocontrast agent, or after the inhibition of prostaglandin or NO synthesis or with their combinations [23]. Outer medullary HIF stabilization is also noted in chronic tubulointerstitial disease [29] and in experi mental diabetes [30], again spatially distributed in areas with proven hypoxia.…”

Section: Hif Expression Under Hypoxic Stress and Tissue Injurysupporting

confidence: 80%

“…HIF-1α and PHD-2 expression increased in the neonatal rat brain following hypoxia [33] and HIF was detected in the hypoxic subendocardium [34] and in the ischemic liver [27]. HIF is also found within hypoxic regions in tumors, and may play an important role in tumor progression via upregulation of growth promoting and angiogenic factors [35].…”

Section: Hif Expression Under Hypoxic Stress and Tissue Injurymentioning

confidence: 99%

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Hypoxia-inducible Factors and the Prevention of Acute Organ Injury

Heyman¹,

Rosen²,

Rosenberger³

2011

Annual Update in Intensive Care and Emergency Medicine 2011

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Section: Hif Expression Under Hypoxic Stress and Tissue Injurysupporting

confidence: 80%

Section: Hif Expression Under Hypoxic Stress and Tissue Injurymentioning

confidence: 99%

Hypoxia-inducible Factors and the Prevention of Acute Organ Injury

Heyman¹,

Rosen²,

Rosenberger³

2011

Annual Update in Intensive Care and Emergency Medicine 2011

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“…Thus this sequence of events seems similar to what is seen with IR insults (72)(73)(74)(75). First, it is known that IR injury induces increased expression of the transcription factor HIF-1␣ in tissues such as liver (32). HIF-1␣ levels are greater in placental tissue from preeclamptic versus normal pregnant women (140).…”

Section: Effects Of Obesity On the Placental Function And Perfusionsupporting

confidence: 52%

Increased risk for the development of preeclampsia in obese pregnancies: weighing in on the mechanisms

Spradley

Palei

Granger

2015

American Journal of Physiology-Regulatory, Integrative and Comp

108

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) is a pregnancy-specific disorder typically presenting as new-onset hypertension and proteinuria. While numerous epidemiological studies have demonstrated that obesity increases the risk of PE, the mechanisms have yet to be fully elucidated. Growing evidence from animal and human studies implicate placental ischemia in the etiology of this maternal syndrome. It is thought that placental ischemia is brought about by dysfunctional cytotrophoblast migration and invasion into the uterus and subsequent lack of spiral arteriole widening and placental perfusion. Placental ischemia/ hypoxia stimulates the release of soluble placental factors into the maternal circulation where they cause endothelial dysfunction, particularly in the kidney, to elicit the clinical manifestations of PE. The most recognized of these factors are the anti-angiogenic sFlt-1 and pro-inflammatory TNF-␣ and AT1-AA, which promote endothelial dysfunction by reducing levels of the provasodilator nitric oxide and stimulating production of the potent vasoconstrictor endothelin-1 and reactive oxygen species. We hypothesize that obesity-related metabolic factors increase the risk for developing PE by impacting various stages in the pathogenesis of PE, namely, 1) cytotrophoblast migration and placental ischemia; 2) release of soluble placental factors into the maternal circulation; and 3) maternal endothelial and vascular dysfunction. This review will summarize the current experimental evidence supporting the concept that obesity and metabolic factors like lipids, insulin, glucose, and leptin affect placental function and increase the risk for developing hypertension in pregnancy by reducing placental perfusion; enhancing placental release of soluble factors; and by increasing the sensitivity of the maternal vasculature to placental ischemia-induced soluble factors. body mass index; inflammation; placental ischemia; pregnancy; RUPP; sFlt-1 PE IS A PREGNANCY-SPECIFIC DISORDER typically identified by new-onset hypertension in the second half of pregnancy. Although often accompanied by new-onset proteinuria, PE can be associated with many other signs and symptoms including headaches, visual disturbances, epigastric pain, and the development of edema (4,192). Globally, this disease affects over 8 million pregnancies per year and is estimated to account for 40 -60% of maternal deaths in developing countries (125). In the United States, there was a 25% increase in the rate of PE between the years 1987-2004 (189). This significant increase highlights the importance of understanding how risk factors like obesity play a role in the pathogenesis of this maternal syndrome. Obesity is defined as a body mass index (BMI) of greater than or equal to 30 kg/m 2 . Greater than one-half of pregnant women are overweight or obese (48), and more than two-thirds of reproductive-aged women in the United States are overweight or obese (49). Although mounting epidemiological evidence supports obesity as a major risk factor for PE, the mechanisms linking these two morbidities are...

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“…HIF-1␣ has been implicated in hepatocyte death in models of liver injury that have an inflammatory or oxidative stress component, such as sepsis (Peyssonnaux et al, 2007), ischemia/reperfusion (Cursio et al, 2008), alcoholic liver disease (Li et al, 2006), and fibrosis (Copple et al, 2009). Oxidative stress and mitochondrial dysfunction play a key role in acetaminophen [N-acetyl-p-aminophenol (APAP)]-induced liver injury (James et al, 2003).…”

Section: Introductionmentioning

confidence: 99%