Hypoxia (Auckland, N.Z.)最新文献_第6页

Frequently asked questions in hypoxia research 缺氧研究中的常见问题

Hypoxia (Auckland, N.Z.) Pub Date : 2015-09-18 DOI: 10.2147/HP.S92198

R. Wenger, V. Kurtcuoglu, Carsten C. Scholz, H. H. Marti, D. Hoogewijs

引用次数: 160

Resistance of subventricular neural stem cells to chronic hypoxemia despite structural disorganization of the germinal center and impairment of neuronal and oligodendrocyte survival. 尽管生殖中心结构紊乱，神经元和少突胶质细胞存活能力受损，但室管膜下神经干细胞对慢性低氧血症仍有抵抗力。

Hypoxia (Auckland, N.Z.) Pub Date : 2015-06-08 eCollection Date: 2015-01-01 DOI: 10.2147/HP.S78248

Xavier d'Anglemont de Tassigny, M Salomé Sirerol-Piquer, Ulises Gómez-Pinedo, Ricardo Pardal, Sonia Bonilla, Vivian Capilla-Gonzalez, Ivette López-López, Francisco Javier De la Torre-Laviana, José Manuel García-Verdugo, José López-Barneo

{"title":"Resistance of subventricular neural stem cells to chronic hypoxemia despite structural disorganization of the germinal center and impairment of neuronal and oligodendrocyte survival.","authors":"Xavier d'Anglemont de Tassigny, M Salomé Sirerol-Piquer, Ulises Gómez-Pinedo, Ricardo Pardal, Sonia Bonilla, Vivian Capilla-Gonzalez, Ivette López-López, Francisco Javier De la Torre-Laviana, José Manuel García-Verdugo, José López-Barneo","doi":"10.2147/HP.S78248","DOIUrl":"10.2147/HP.S78248","url":null,"abstract":"Chronic hypoxemia, as evidenced in de-acclimatized high-altitude residents or in patients with chronic obstructive respiratory disorders, is a common medical condition that can produce serious neurological alterations. However, the pathogenesis of this phenomenon is unknown. We have found that adult rodents exposed for several days/weeks to hypoxia, with an arterial oxygen tension similar to that of chronically hypoxemic patients, manifest a partially irreversible structural disarrangement of the subventricular neurogenic niche (subventricular zone) characterized by displacement of neurons and myelinated axons, flattening of the ependymal cell layer, and thinning of capillary walls. Despite these abnormalities, the number of neuronal and oligodendrocyte progenitors, neuroblasts, and neurosphere-forming cells as well as the proliferative activity in subventricular zone was unchanged. These results suggest that neural stem cells and their undifferentiated progeny are resistant to hypoxia. However, in vivo and in vitro experiments indicate that severe chronic hypoxia decreases the survival of newly generated neurons and oligodendrocytes, with damage of myelin sheaths. These findings help explain the effects of hypoxia on adult neurogenesis and provide new perspectives on brain responsiveness to persistent hypoxemia.","PeriodicalId":73270,"journal":{"name":"Hypoxia (Auckland, N.Z.)","volume":"3 1","pages":"15-33"},"PeriodicalIF":0.0,"publicationDate":"2015-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5045070/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68361555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Therapeutic inhibition of prolyl hydroxylase domain-containing enzymes in surgery: putative applications and challenges 手术中含有脯氨酰羟化酶结构域的酶的治疗抑制:推测的应用和挑战

Hypoxia (Auckland, N.Z.) Pub Date : 2015-01-30 DOI: 10.2147/HP.S60872

J. Harnoss, Moritz J. Strowitzki, P. Radhakrishnan, L. K. Platzer, J. Harnoss, T. Hank, Jun Cai, A. Ulrich, Martin Schneider

引用次数: 26

Signaling hypoxia by hypoxia-inducible factor protein hydroxylases: a historical overview and future perspectives 缺氧诱导因子蛋白羟化酶的缺氧信号:历史回顾和未来展望

Hypoxia (Auckland, N.Z.) Pub Date : 2014-12-05 DOI: 10.2147/HP.S47598

T. Bishop, P. Ratcliffe

{"title":"Signaling hypoxia by hypoxia-inducible factor protein hydroxylases: a historical overview and future perspectives","authors":"T. Bishop, P. Ratcliffe","doi":"10.2147/HP.S47598","DOIUrl":"https://doi.org/10.2147/HP.S47598","url":null,"abstract":"By the early 1900s, the close matching of oxygen supply with demand was recognized to be a fundamental requirement for physiological function, and multiple adaptive responses to environment hypoxia had been described. Nevertheless, the widespread operation of mechanisms that directly sense and respond to levels of oxygen in animal cells was not appreciated for most of the twentieth century with investigators generally stressing the regulatory importance of metabolic products. Work over the last 25 years has overturned that paradigm. It has revealed the existence of a set of “oxygen-sensing” 2-oxoglutarate dependent dioxygenases that catalyze the hydroxylation of specific amino acid residues and thereby control the stability and activity of hypoxia-inducible factor. The hypoxia-inducible factor hydroxylase pathway regulates a massive transcriptional cascade that is operative in essentially all animal cells. It transduces a wide range of responses to hypoxia, extending well beyond the classical boundaries of hypoxia physiology. Here we review the discovery and elucidation of these pathways, and consider the opportunities and challenges that have been brought into focus by the findings, including new implications for the integrated physiology of hypoxia and therapeutic approaches to ischemic/hypoxic disease.","PeriodicalId":73270,"journal":{"name":"Hypoxia (Auckland, N.Z.)","volume":"2 1","pages":"197 - 213"},"PeriodicalIF":0.0,"publicationDate":"2014-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/HP.S47598","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68360795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 39

Macrophage-mediated response to hypoxia in disease 巨噬细胞介导的疾病缺氧反应

Hypoxia (Auckland, N.Z.) Pub Date : 2014-11-15 DOI: 10.2147/HP.S49717

S. Tazzyman, C. Murdoch, J. Yeomans, Jack Harrison, M. Muthana

{"title":"Macrophage-mediated response to hypoxia in disease","authors":"S. Tazzyman, C. Murdoch, J. Yeomans, Jack Harrison, M. Muthana","doi":"10.2147/HP.S49717","DOIUrl":"https://doi.org/10.2147/HP.S49717","url":null,"abstract":"Hypoxia plays a critical role in the pathobiology of various inflamed, diseased tissues, including malignant tumors, atherosclerotic plaques, myocardial infarcts, the synovia of rheumatoid arthritic joints, healing wounds, and sites of bacterial infection. These areas of hypoxia form when the blood supply is occluded and/or the oxygen supply is unable to keep pace with cell growth and/or infiltration of inflammatory cells. Macrophages are ubiquitous in all tissues of the body and exhibit great plasticity, allowing them to perform divergent functions, including, among others, patrolling tissue, combating invading pathogens and tumor cells, orchestrating wound healing, and restoring homeostasis after an inflammatory response. The number of tissue macrophages increases markedly with the onset and progression of many pathological states, with many macrophages accumulating in avascular and necrotic areas, where they are exposed to hypoxia. Recent studies show that these highly versatile cells then respond rapidly to the hypoxia present by altering their expression of a wide array of genes. Here we review the evidence for hypoxia-driven macrophage inflammatory responses in various disease states, and how this influences disease progression and treatment.","PeriodicalId":73270,"journal":{"name":"Hypoxia (Auckland, N.Z.)","volume":"2 1","pages":"185 - 196"},"PeriodicalIF":0.0,"publicationDate":"2014-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/HP.S49717","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68360829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 11

Regulation of obesity and insulin resistance by hypoxia-inducible factors 低氧诱导因子对肥胖和胰岛素抵抗的调节

Hypoxia (Auckland, N.Z.) Pub Date : 2014-11-13 DOI: 10.2147/HP.S68771

J. Ban, Robin J. Ruthenborg, Kevin w Cho, Jung-whan Kim

引用次数: 42

Effects of copper sulfate-oxidized or myeloperoxidase-modified LDL on lipid loading and programmed cell death in macrophages under hypoxia. 硫酸铜氧化或髓过氧化物酶修饰的低密度脂蛋白对缺氧条件下巨噬细胞脂质负荷和程序性细胞死亡的影响

Hypoxia (Auckland, N.Z.) Pub Date : 2014-09-23 eCollection Date: 2014-01-01 DOI: 10.2147/HP.S65242

Benoit Vlaminck, Damien Calay, Marie Genin, Aude Sauvage, Noelle Ninane, Karim Zouaoui Boudjeltia, Martine Raes, Carine Michiels

{"title":"Effects of copper sulfate-oxidized or myeloperoxidase-modified LDL on lipid loading and programmed cell death in macrophages under hypoxia.","authors":"Benoit Vlaminck, Damien Calay, Marie Genin, Aude Sauvage, Noelle Ninane, Karim Zouaoui Boudjeltia, Martine Raes, Carine Michiels","doi":"10.2147/HP.S65242","DOIUrl":"10.2147/HP.S65242","url":null,"abstract":"Atheromatous plaques contain heavily lipid-loaded macrophages that die, hence generating the necrotic core of these plaques. Since plaque instability and rupture is often correlated with a large necrotic core, it is important to understand the mechanisms underlying foam cell death. Furthermore, macrophages within the plaque are associated with hypoxic areas but little is known about the effect of low oxygen partial pressure on macrophage death. The aim of this work was to unravel macrophage death mechanisms induced by oxidized low-density lipoproteins (LDL) both under normoxia and hypoxia. Differentiated macrophages were incubated in the presence of native, copper sulfate-oxidized, or myeloperoxidase-modified LDL. The unfolded protein response, apoptosis, and autophagy were then investigated. The unfolded protein response and autophagy were triggered by myeloperoxidase-modified LDL and, to a larger extent, by copper sulfate-oxidized LDL. Electron microscopy observations showed that oxidized LDL induced excessive autophagy and apoptosis under normoxia, which were less marked under hypoxia. Myeloperoxidase-modified LDL were more toxic and induced a higher level of apoptosis. Hypoxia markedly decreased apoptosis and cell death, as marked by caspase activation. In conclusion, the cell death pathways induced by copper sulfate-oxidized and myeloperoxidase-modified LDL are different and are differentially modulated by hypoxia.","PeriodicalId":73270,"journal":{"name":"Hypoxia (Auckland, N.Z.)","volume":"2 1","pages":"153-169"},"PeriodicalIF":0.0,"publicationDate":"2014-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5045064/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68361265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Arginine-vasopressin marker copeptin is a sensitive plasma surrogate of hypoxic exposure 精氨酸-抗利尿激素标志物copeptin是缺氧暴露的敏感血浆替代物

Hypoxia (Auckland, N.Z.) Pub Date : 2014-09-11 DOI: 10.2147/HP.S57894

L. Ostergaard, A. Rudiger, S. Wellmann, Elena Gammella, B. Beck-Schimmer, J. Struck, M. Maggiorini, M. Gassmann

{"title":"Arginine-vasopressin marker copeptin is a sensitive plasma surrogate of hypoxic exposure","authors":"L. Ostergaard, A. Rudiger, S. Wellmann, Elena Gammella, B. Beck-Schimmer, J. Struck, M. Maggiorini, M. Gassmann","doi":"10.2147/HP.S57894","DOIUrl":"https://doi.org/10.2147/HP.S57894","url":null,"abstract":"Background A reduced oxygen supply puts patients at risk of tissue hypoxia, organ damage, and even death. In response, several changes are activated that allow for at least partial adaptation, thereby increasing the chances of survival. We aimed to investigate whether the arginine vasopressin marker, copeptin, can be used as a marker of the degree of acclimatization/adaptation in rats exposed to hypoxia. Methods Sprague-Dawley rats were exposed to 10% oxygen for up to 48 hours. Arterial and right ventricular pressures were measured, and blood gas analysis was performed at set time points. Pulmonary changes were investigated by bronchoalveolar lavage, wet and dry weight measurements, and lung histology. Using a newly developed specific rat copeptin luminescence immunoassay, the regulation of vasopressin in response to hypoxia was studied, as was atrial natriuretic peptide (ANP) by detecting mid-regional proANP. Results With a decreasing oxygen supply, the rats rapidly became cyanotic and inactive. Despite continued exposure to 10% oxygen, all animals recuperated within 16 hours and ultimately survived. Their systemic blood pressure fell with acute (5 minutes) hypoxia but was partially recovered over time. In contrast, right ventricular pressures increased with acute (5 minutes) hypoxia and normalized after 16 hours. No signs of pulmonary inflammation or edema were found despite prolonged hypoxia. Whereas copeptin levels increased significantly after acute (5 minutes) hypoxia and then returned to near baseline after 16 hours, mid-regional proANP levels were even further increased after 16 hours of exposure to hypoxia. Conclusion Plasma copeptin is a sensitive marker of acute (5 minutes) exposure to severe hypoxia, and subsequent regulation can indicate recovery. Copeptin levels can therefore reflect clinical and physiological changes in response to hypoxia and indicate recovery from ongoing hypoxic exposure.","PeriodicalId":73270,"journal":{"name":"Hypoxia (Auckland, N.Z.)","volume":"2 1","pages":"143 - 151"},"PeriodicalIF":0.0,"publicationDate":"2014-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/HP.S57894","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68360659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 14

Prolyl hydroxylase domain enzymes: important regulators of cancer metabolism 脯氨酸羟化酶结构域酶:肿瘤代谢的重要调节因子

Hypoxia (Auckland, N.Z.) Pub Date : 2014-08-30 DOI: 10.2147/HP.S47968

Ming Yang, Huizhong Su, T. Soga, Kamil R. Kranc, Patrick J. Pollard

{"title":"Prolyl hydroxylase domain enzymes: important regulators of cancer metabolism","authors":"Ming Yang, Huizhong Su, T. Soga, Kamil R. Kranc, Patrick J. Pollard","doi":"10.2147/HP.S47968","DOIUrl":"https://doi.org/10.2147/HP.S47968","url":null,"abstract":"The hypoxia-inducible factor (HIF) prolyl hydroxylase domain enzymes (PHDs) regulate the stability of HIF protein by post-translational hydroxylation of two conserved prolyl residues in its α subunit in an oxygen-dependent manner. Trans-4-prolyl hydroxylation of HIFα under normal oxygen (O2) availability enables its association with the von Hippel-Lindau (VHL) tumor suppressor pVHL E3 ligase complex, leading to the degradation of HIFα via the ubiquitin-proteasome pathway. Due to the obligatory requirement of molecular O2 as a co-substrate, the activity of PHDs is inhibited under hypoxic conditions, resulting in stabilized HIFα, which dimerizes with HIFβ and, together with transcriptional co-activators CBP/p300, activates the transcription of its target genes. As a key molecular regulator of adaptive response to hypoxia, HIF plays important roles in multiple cellular processes and its overexpression has been detected in various cancers. The HIF1α isoform in particular has a strong impact on cellular metabolism, most notably by promoting anaerobic, whilst inhibiting O2-dependent, metabolism of glucose. The PHD enzymes also seem to have HIF-independent functions and are subject to regulation by factors other than O2, such as by metabolic status, oxidative stress, and abnormal levels of endogenous metabolites (oncometabolites) that have been observed in some types of cancers. In this review, we aim to summarize current understandings of the function and regulation of PHDs in cancer with an emphasis on their roles in metabolism.","PeriodicalId":73270,"journal":{"name":"Hypoxia (Auckland, N.Z.)","volume":"2 1","pages":"127 - 142"},"PeriodicalIF":0.0,"publicationDate":"2014-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2147/HP.S47968","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68360825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 38

Modulation of hydrogen sulfide by vascular hypoxia 血管缺氧对硫化氢的调节

Hypoxia (Auckland, N.Z.) Pub Date : 2014-08-25 DOI: 10.2147/HP.S51589

J. Osmond, N. Kanagy

引用次数: 7