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Journal articles on the topic 'Hypoxia-Inducible'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Aldecoa Bedoya, Franklin. "Factor inducible por hipoxia en cáncer." Horizonte Médico (Lima) 23, no. 4 (2023): e2584. http://dx.doi.org/10.24265/horizmed.2023.v23n4.11.

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2

Liu, Ting, Le Zhao, Huilian Hou, Lu Ding, Wei Chen, and Xu Li. "Ginsenoside 20(S)-Rg3 suppresses ovarian cancer migration via hypoxia-inducible factor 1 alpha and nuclear factor-kappa B signals." Tumor Biology 39, no. 5 (2017): 101042831769222. http://dx.doi.org/10.1177/1010428317692225.

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Hypoxia-inducible factor 1 is believed to play a prominent role in the survival and developing progress of cancers. As a result, inhibiting α subunit of hypoxia-inducible factor 1 represents an attractive strategy against tumor. Although hypoxia-inducible factor 1α is a hypoxia-regulated subunit, increasing evidence indicates that hypoxia-inducible factor 1α could stable expression under normoxic conditions, regulated by non-hypoxia-mediated mechanisms. However, there are few strategies to target hypoxia-inducible factor 1α under normoxic conditions. Here, we report that ginsenoside 20(S)-Rg3,

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3

Sang, Xiguang, Zhiyong Wang, Tao Qin та Yonggang Li. "Elevated concentrations of hypoxia-inducible factor-1α in patients with fracture and concomitant traumatic brain injury". Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 54, № 5 (2016): 584–92. http://dx.doi.org/10.1177/0004563216673087.

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Background Compelling evidence indicate that traumatic brain injury is highly related to accelerated bone fracture repair, but the underlying mechanism still remains elusive. Fracture repair process relies greatly on the formation of new blood vessels in fracture site, and angiogenic factors have been confirmed to be essential for the initiation and maintenance of the fracture healing. Hypoxia-inducible factor-1α was demonstrated to be a critical regulator of angiogenic–osteogenic coupling during bone development and regeneration. The aim of the present study was to investigate the local and c

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4

kun, Zhang, Yang yuling, Wang dongchun, Xie bingbing, Li xiaoli та Xu bin. "HIF-1α Inhibition Sensitized Pituitary Adenoma Cells to Temozolomide by Regulating Presenilin 1 Expression and Autophagy". Technology in Cancer Research & Treatment 15, № 6 (2016): NP95—NP104. http://dx.doi.org/10.1177/1533034615618834.

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Pituitary adenomas usually develop temozolomide resistance, which could compromise the anticancer effects of temozolomide. Suppression of hypoxia-inducible factor 1α has been shown to sensitize glioblastoma cells to temozolomide treatment according to previous reports. However, whether and how the suppression of hypoxia-inducible factor 1α could sensitize pituitary adenomas to temozolomide treatment are still poorly understood. In the present study, using hypoxia-inducible factor 1α knockdown strategy, we demonstrated for the first time that hypoxia-inducible factor 1α knockdown could inhibit

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5

Walmsley, Sarah R., Edwin R. Chilvers, and Moira KB Whyte. "Hypoxia. Hypoxia, hypoxia inducible factor and myeloid cell function." Arthritis Research & Therapy 11, no. 2 (2009): 219. http://dx.doi.org/10.1186/ar2632.

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6

Pan, Fan, Joseph Barbi, and Drew M. Pardoll. "Hypoxia-inducible factor 1." OncoImmunology 1, no. 4 (2012): 510–15. http://dx.doi.org/10.4161/onci.19457.

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7

Semenza, Gregg L., Faton Agani, Narayan Iyer, et al. "Hypoxia-Inducible Factor 1." Chest 114, no. 1 (1998): 40S—45S. http://dx.doi.org/10.1378/chest.114.1_supplement.40s.

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8

Tsuchiya, T. "Hypoxia-inducible transcriptional cofactor." Neuroscience Research 38 (2000): S40. http://dx.doi.org/10.1016/s0168-0102(00)81086-x.

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9

Fandrey, Joachim. "Hypoxia-inducible gene expression." Respiration Physiology 101, no. 1 (1995): 1–10. http://dx.doi.org/10.1016/0034-5687(95)00013-4.

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10

Lee, Kyoung Eun, and M. Celeste Simon. "SnapShot: Hypoxia-Inducible Factors." Cell 163, no. 5 (2015): 1288–1288. http://dx.doi.org/10.1016/j.cell.2015.11.011.

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11

Choudhry, H. "Effect of Hypoxia Inducible Factor on Hypoxia Inducible Gene Expression and Glycolysis." Journal of Advances in Medical and Pharmaceutical Sciences 11, no. 3 (2016): 1–10. http://dx.doi.org/10.9734/jamps/2016/29407.

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12

Foglia, Beatrice, Erica Novo, Francesca Protopapa, et al. "Hypoxia, Hypoxia-Inducible Factors and Liver Fibrosis." Cells 10, no. 7 (2021): 1764. http://dx.doi.org/10.3390/cells10071764.

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Liver fibrosis is a potentially reversible pathophysiological event, leading to excess deposition of extracellular matrix (ECM) components and taking place as the net result of liver fibrogenesis, a dynamic and highly integrated process occurring during chronic liver injury of any etiology. Liver fibrogenesis and fibrosis, together with chronic inflammatory response, are primarily involved in the progression of chronic liver diseases (CLD). As is well known, a major role in fibrogenesis and fibrosis is played by activated myofibroblasts (MFs), as well as by macrophages and other hepatic cell p

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13

Karhausen, Jörn, Volker H. Haase, and Sean P. Colgan. "Inflammatory Hypoxia: Role of Hypoxia-Inducible Factor." Cell Cycle 4, no. 2 (2004): 255–57. http://dx.doi.org/10.4161/cc.4.2.1407.

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14

Påhlman, Sven, and Sofie Mohlin. "Hypoxia and hypoxia-inducible factors in neuroblastoma." Cell and Tissue Research 372, no. 2 (2017): 269–75. http://dx.doi.org/10.1007/s00441-017-2701-1.

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15

Gruber, Michaela, and M. Celeste Simon. "Hypoxia-inducible factors, hypoxia, and tumor angiogenesis." Current Opinion in Hematology 13, no. 3 (2006): 169–74. http://dx.doi.org/10.1097/01.moh.0000219663.88409.35.

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16

Agena, S., H. Hirakawa, T. Ikegami та ін. "Prognostic significance of hypoxia-inducible factor-1α expression in advanced pharyngeal cancer without human papillomavirus infection". Journal of Laryngology & Otology 135, № 7 (2021): 625–33. http://dx.doi.org/10.1017/s0022215121001468.

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AbstractObjectiveThis study aimed to clarify the association between both hypoxia-inducible factor-1α and glucose transporter type-1 expression and survival outcome in advanced pharyngeal cancer without human papillomavirus infection.MethodTwenty-five oropharyngeal and 55 hypopharyngeal cancer patients without human papillomavirus infection were enrolled. All patients had stage III–IV lesions and underwent concurrent chemoradiotherapy or surgery. Hypoxia-inducible factor-1α and glucose transporter type-1 expression were investigated in primary lesions by immunohistochemistry.ResultsThere were

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17

Østergaard, Louise, and Max Gassmann. "Hypoxia Inducible Factor and Hypoxia-mediated Pulmonary Hypertension." PVRI Review 3, no. 1 (2011): 5. http://dx.doi.org/10.4103/0974-6013.85613.

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18

Zeng, Wen, Peiyi Liu, Weimin Pan, Shree Ram Singh, and Yiyong Wei. "Hypoxia and hypoxia inducible factors in tumor metabolism." Cancer Letters 356, no. 2 (2015): 263–67. http://dx.doi.org/10.1016/j.canlet.2014.01.032.

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19

Nangaku, Masaomi, Reiko Inagi, Toshio Miyata, and Toshiro Fujita. "Hypoxia and Hypoxia-Inducible Factor in Renal Disease." Nephron Experimental Nephrology 110, no. 1 (2008): e1-e7. http://dx.doi.org/10.1159/000148256.

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20

Schödel, Johannes, Steffen Grampp, Eamonn R. Maher, et al. "Hypoxia, Hypoxia-inducible Transcription Factors, and Renal Cancer." European Urology 69, no. 4 (2016): 646–57. http://dx.doi.org/10.1016/j.eururo.2015.08.007.

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21

Greenwood, Krista K., Steven P. Proper, Yogesh Saini та ін. "Neonatal epithelial hypoxia inducible factor-1α expression regulates the response of the lung to experimental asthma". American Journal of Physiology-Lung Cellular and Molecular Physiology 302, № 5 (2012): L455—L462. http://dx.doi.org/10.1152/ajplung.00193.2011.

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Allergic airway disease is characterized by a T helper type 2 cell-mediated airway inflammation and airway hyperresponsiveness. Little is known about the role of hypoxia-mediated signaling in the progression of the disease. To address this knowledge gap, a mouse model was created in which doxycycline exposure induces the functional deletion of hypoxia inducible factor-1α from alveolar type II and Clara cells of the lung. When hypoxia inducible factor-1α deletion was induced during the early postnatal development period of the lung, the mice displayed an enhanced response to the ovalbumin model

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22

Shin, Dong Hoon, Shan Hua Li, Seung-Won Yang, Byung Lan Lee, Myung Kyu Lee та Jong-Wan Park. "Inhibitor of nuclear factor-kappaB alpha derepresses hypoxia-inducible factor-1 during moderate hypoxia by sequestering factor inhibiting hypoxia-inducible factor from hypoxia-inducible factor 1α". FEBS Journal 276, № 13 (2009): 3470–80. http://dx.doi.org/10.1111/j.1742-4658.2009.07069.x.

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23

Cha, Ryota, Shuji Nakagawa, Yuji Arai та ін. "Intermittent hypoxic stimulation promotes efficient expression of Hypoxia-inducible factor-1α and exerts a chondroprotective effect in an animal osteoarthritis model". PLOS ONE 20, № 4 (2025): e0319976. https://doi.org/10.1371/journal.pone.0319976.

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Hypoxia-inducible factor-1α plays an important role in the homeostasis of articular cartilage in hypoxic environments. Therefore, modulation of hypoxia-inducible factor-1α by regulating the oxygen environment could be a useful treatment for osteoarthritis. This study aimed to assess the chondroprotective effects of intermittent hypoxia on cultured chondrocytes and an animal model of osteoarthritis. In vitro, human chondrocytes were exposed to 2 h of hypoxic stimulation three times at 1-h intervals, and protein and gene expression of hypoxia-inducible factor-1α, ACAN, and cell viability was mea

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24

del Peso, Luis. "Hypoxia-inducible factor and cancer." Revista de Oncología 6, no. 1 (2004): 3–11. http://dx.doi.org/10.1007/bf02710296.

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25

Kim, Laura C., and M. Celeste Simon. "Hypoxia-Inducible Factors in Cancer." Cancer Research 82, no. 2 (2022): 195–96. http://dx.doi.org/10.1158/0008-5472.can-21-3780.

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26

Guerre-Millo, Michèle, Alexandra Grosfeld, and Tarik Issad. "LeptinIs a Hypoxia-Inducible Gene." Obesity Research 10, no. 8 (2002): 856. http://dx.doi.org/10.1038/oby.2002.116.

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27

DePavia, Adela, Eric Jonasch, and Xian-De Liu. "Autophagy degrades hypoxia inducible factors." Molecular & Cellular Oncology 3, no. 2 (2016): e1104428. http://dx.doi.org/10.1080/23723556.2015.1104428.

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28

Calzada, M. J., and L. del Peso. "Hypoxia-inducible factors and cancer." Clinical and Translational Oncology 9, no. 5 (2007): 278–89. http://dx.doi.org/10.1007/s12094-007-0055-y.

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29

Jun, Jonathan C., Aman Rathore, Haris Younas, Daniele Gilkes, and Vsevolod Y. Polotsky. "Hypoxia-Inducible Factors and Cancer." Current Sleep Medicine Reports 3, no. 1 (2017): 1–10. http://dx.doi.org/10.1007/s40675-017-0062-7.

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30

Pérez-Sayáns, Mario, José Manuel Suárez-Peñaranda, Gayoso-Diz Pilar, Francisco Barros-Angueira, José Manuel Gándara-Rey, and Abel García-García. "Hypoxia-inducible factors in OSCC." Cancer Letters 313, no. 1 (2011): 1–8. http://dx.doi.org/10.1016/j.canlet.2011.08.017.

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31

Gunton, Jenny E. "Hypoxia-inducible factors and diabetes." Journal of Clinical Investigation 130, no. 10 (2020): 5063–73. http://dx.doi.org/10.1172/jci137556.

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32

Amin, Nashwa, Shijia Chen, Qiannan Ren та ін. "Hypoxia Inducible Factor-1α Attenuates Ischemic Brain Damage by Modulating Inflammatory Response and Glial Activity". Cells 10, № 6 (2021): 1359. http://dx.doi.org/10.3390/cells10061359.

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Hypoxia-inducible factor 1 can sufficiently control the progress of neurological symptoms after ischemic stroke owing to their actions associated with its downstream genes. In this study, we evaluated the role of HIF-1α in attenuating brain damage after endothelin-1 injection. Focal cerebral ischemia in mice were induced by endothelin-1 microinjection. Hypoxia-inducible factor 1 activator, dimethyloxalylglycine (DMOG), and HIF-1α inhibitor, acriflavine (ACF), were used to evaluate the hypoxia-inducible factor 1 activity during cerebral ischemia. The expression levels of HIF-1α, glial fibrillar

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33

Sparkle, Tanaya. "Roxadustat: A Narrative Review of Action and Safety Profile." Anesthesia & Clinical Care 9, no. 1 (2022): 1–8. http://dx.doi.org/10.24966/acc-8879/100072.

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Hypoxia-inducible factor prolyl hydroxylase inhibitors are a relatively new class of drugs that act by inhibiting the enzyme hypoxia-inducible factor-proline dioxygenase (HIF prolyl-hydroxylase or HIF-PHD).

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34

López‐Lázaro, Miguel. "HIF‐1: hypoxia‐inducible factor or dysoxia‐inducible factor?" FASEB Journal 20, no. 7 (2006): 828–32. http://dx.doi.org/10.1096/fj.05-5168hyp.

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35

Terker, Andrew S., Kensuke Sasaki, Juan Pablo Arroyo, et al. "Activation of hypoxia-sensing pathways promotes renal ischemic preconditioning following myocardial infarction." American Journal of Physiology-Renal Physiology 320, no. 4 (2021): F569—F577. http://dx.doi.org/10.1152/ajprenal.00476.2020.

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Experimental myocardial infarction (MI) protects from subsequent ischemic acute kidney injury but worsens chronic kidney injury. Observed protection from ischemic acute kidney injury after MI was accompanied by chronic kidney hypoxia and increased renal abundance of hypoxia-inducible transcripts. These data support the idea that MI confers protection from renal ischemic injury via chronic renal hypoxia and activation of downstream hypoxia-inducible signaling pathways.

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36

Chen, Ruoli, and Halimatu Hassan. "Hypoxia in Alzheimer's disease: effects of hypoxia inducible factors." Neural Regeneration Research 16, no. 2 (2021): 310. http://dx.doi.org/10.4103/1673-5374.290898.

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37

Xing, Dongmei, Lixin Liu, Guy P. Marti, et al. "Hypoxia and hypoxia-inducible factor in the burn wound." Wound Repair and Regeneration 19, no. 2 (2011): 205–13. http://dx.doi.org/10.1111/j.1524-475x.2010.00656.x.

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38

Schipani, Ernestina, and Thomas L. Clemens. "Hypoxia and the hypoxia-inducible factors in the skeleton." IBMS BoneKEy 5, no. 8 (2008): 275–84. http://dx.doi.org/10.1138/20080329.

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39

Douglas, N., H. Tang, G. S. Nakhuda, M. Sauer, and R. Zimmermann. "Oocyte Expression of Hypoxia and Hypoxia Inducible Factors (HIF)." Fertility and Sterility 84 (September 2005): S390. http://dx.doi.org/10.1016/j.fertnstert.2005.07.1020.

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40

Lu, Xin, and Yibin Kang. "Hypoxia and Hypoxia-Inducible Factors: Master Regulators of Metastasis." Clinical Cancer Research 16, no. 24 (2010): 5928–35. http://dx.doi.org/10.1158/1078-0432.ccr-10-1360.

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41

Zimmer, Michael, Darrell Doucette, Naila Siddiqui, and Othon Iliopoulos. "Inhibition of Hypoxia-Inducible Factor Is Sufficient for Growth Suppression of VHL−/− Tumors." Molecular Cancer Research 2, no. 2 (2004): 89–95. http://dx.doi.org/10.1158/1541-7786.89.2.2.

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Abstract The von Hippel-Lindau tumor suppressor protein (pVHL) is a substrate receptor for the mammalian SCF-2 E3 ubiquitin ligase complex that targets several substrates for ubiquitination and proteasomal degradation. Among these targets are the α-regulatory subunits of the hypoxia-inducible factor (HIF). VHL−/− cells constitutively overexpress hypoxia-inducible genes through both transcriptional and posttranscriptional mechanisms and form tumors when injected into nude mice. Reintroduction of pVHL into VHL−/− cell lines restores normal oxygen-dependent regulation of these genes and suppresse

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42

Irigoyen, Marta, Juan Carlos García-Ruiz, and Edurne Berra. "The hypoxia signalling pathway in haematological malignancies." Oncotarget 8, no. 22 (2017): 36832–44. https://doi.org/10.18632/oncotarget.15981.

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Haematological malignancies are tumours that affect the haematopoietic and the lymphatic systems. Despite the huge efforts to eradicate these tumours, the percentage of patients suffering resistance to therapies and relapse still remains significant. The tumour environment favours drug resistance of cancer cells, and particularly of cancer stem/initiating cells. Hypoxia promotes aggressiveness, metastatic spread and relapse in most of the solid tumours. Furthermore, hypoxia is associated with worse prognosis and resistance to conventional treatments through activation of the hypoxia-inducible

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43

Ono, Yoko, and Hidemasa Bono. "Multi-Omic Meta-Analysis of Transcriptomes and the Bibliome Uncovers Novel Hypoxia-Inducible Genes." Biomedicines 9, no. 5 (2021): 582. http://dx.doi.org/10.3390/biomedicines9050582.

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Hypoxia is a condition in which cells, tissues, or organisms are deprived of sufficient oxygen supply. Aerobic organisms have a hypoxic response system, represented by hypoxia-inducible factor 1-α (HIF1A), to adapt to this condition. Due to publication bias, there has been little focus on genes other than well-known signature hypoxia-inducible genes. Therefore, in this study, we performed a meta-analysis to identify novel hypoxia-inducible genes. We searched publicly available transcriptome databases to obtain hypoxia-related experimental data, retrieved the metadata, and manually curated it.

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44

Lee, Jae W., Michael Koeppen, Seong-Wook Seo, et al. "Transcription-independent Induction of ERBB1 through Hypoxia-inducible Factor 2A Provides Cardioprotection during Ischemia and Reperfusion." Anesthesiology 132, no. 4 (2020): 763–80. http://dx.doi.org/10.1097/aln.0000000000003037.

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Abstract Background During myocardial ischemia, hypoxia-inducible factors are stabilized and provide protection from ischemia and reperfusion injury. Recent studies show that myocyte-specific hypoxia-inducible factor 2A promotes myocardial ischemia tolerance through induction of epidermal growth factor, amphiregulin. Here, the authors hypothesized that hypoxia-inducible factor 2A may enhance epidermal growth factor receptor 1 (ERBB1) expression in the myocardium that could interface between growth factors and its effect on providing tolerance to ischemia and reperfusion injury. Methods Human m

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45

Ajaz, Ahmad Waza* Shabir Ahmad Bhat Zeenat Hamid. "TARGETING HIF-1 PATHWAY: A THERAPEUTIC APPROACH TO KILL CANCER CELLS." Indo American Journal of Pharmaceutical Sciences 04, no. 11 (2017): 4088–93. https://doi.org/10.5281/zenodo.1048230.

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Tumorous growth often faces hypoxic (low oxygen tension) conditions and the adaptations of these cells to hypoxic conditions determine their survival. The cancer cells respond to hypoxia by altering the expression of different genes and Hypoxia-Inducible Factor (HIF)-1 is one of it. HIF-1 is a transcriptional factor that response to hypoxia (low oxygen tension) conditions quickly. Expression of HIF-1 gene is essential for increase in vascularization of hypoxic region such as tumor and thus aid in proliferation and survival of cancerous cells. Moreover, HIF-1 signaling in cancer cells has a div

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46

Kozal, Karolina, and Anna Krześlak. "The Role of Hypoxia-Inducible Factor Isoforms in Breast Cancer and Perspectives on Their Inhibition in Therapy." Cancers 14, no. 18 (2022): 4518. http://dx.doi.org/10.3390/cancers14184518.

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Hypoxia is a common feature associated with many types of cancer. The activity of the hypoxia-inducible factors (HIFs), the critical element of response and adaptation to hypoxia, enhances cancer hallmarks such as suppression of the immune response, altered metabolism, angiogenesis, invasion, metastasis, and more. The HIF-1α and HIF-2α isoforms show similar regulation characteristics, although they are active in different types of hypoxia and can show different or even opposite effects. Breast cancers present several unique ways of non-canonical hypoxia-inducible factors activity induction, no

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47

Burrows, Natalie, Muhammad Babur, Julia Resch, Kaye J. Williams, and Georg Brabant. "Hypoxia-Inducible Factor in Thyroid Carcinoma." Journal of Thyroid Research 2011 (2011): 1–17. http://dx.doi.org/10.4061/2011/762905.

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Intratumoural hypoxia (low oxygen tension) is associated with aggressive disease and poor prognosis. Hypoxia-inducible factor-1 is a transcription factor activated by hypoxia that regulates the expression of genes that promote tumour cell survival, progression, metastasis, and resistance to chemo/radiotherapy. In addition to hypoxia, HIF-1 can be activated by growth factor-signalling pathways such as the mitogen-activated protein kinases- (MAPK-) and phosphatidylinositol-3-OH kinases- (PI3K-) signalling cascades. Mutations in these pathways are common in thyroid carcinoma and lead to enhanced

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48

Shevchenko, N. S., N. V. Krutenko, T. V. Zimnytska, and K. V. Voloshyn. "The role of hypoxia-inducible factors in the development of chronic pathology." Ukrainian Biochemical Journal 93, no. 4 (2021): 18–25. http://dx.doi.org/10.15407/ubj93.04.018.

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This review highlights the current understanding of hypoxia-inducible factors (HIFs) role as regulators of oxygen-dependent reactions and inducers of genes expression in human organism. The focus is on the most significant relationships between the activation or inhibition of the HIFs intracellular system and development of the inflammatory process in various organs, chronic diseases of gastrointestinal tract, osteoarticular system, kidneys as well as hematological, endocrine and metabolic disorders.

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49

Khan, Zahida, George K. Michalopoulos, and Donna Beer Stolz. "Peroxisomal Localization of Hypoxia-Inducible Factors and Hypoxia-Inducible Factor Regulatory Hydroxylases in Primary Rat Hepatocytes Exposed to Hypoxia-Reoxygenation." American Journal of Pathology 169, no. 4 (2006): 1251–69. http://dx.doi.org/10.2353/ajpath.2006.060360.

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50

Jin, Zicheng, Kai Qu, Ziqing Zhang, and Renwei Zhao. "Progress in the Study of the Therapeutic Effects of Roxarestat." Journal of Contemporary Medical Practice 6, no. 10 (2024): 17–21. http://dx.doi.org/10.53469/jcmp.2024.06(10).04.

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Hypoxia-inducible factor has a wide range of roles in the human body and is involved in pathophysiological processes including erythropoietin production, iron uptake metabolism and energy metabolism. Roxarestat is a small molecule inhibitor of hypoxia-inducible factor prolyl hydroxylase, which can stabilize the level of hypoxia-inducible factor to participate in systemic biological functions. Roxarestat is widely used in the treatment of renal anemia. With the deepening of research, it is found that roxarestat has therapeutic potential for renal fibrosis, cardiovascular disease, retinopathy, e

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