Hypoxia-Inducible Factors

Oxygen is an essential molecule in the production of adenosine triphosphate (ATP) in cells, and a lack of energy due to O2 deficiency makes the maintenance of biological functions and human life improbable. Since oxygen functions as the final electron acceptor in the series of ATP synthesis reaction...

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description Oxygen is an essential molecule in the production of adenosine triphosphate (ATP) in cells, and a lack of energy due to O2 deficiency makes the maintenance of biological functions and human life improbable. Since oxygen functions as the final electron acceptor in the series of ATP synthesis reactions in conjunction with oxidative phosphorylation in mitochondria, its deficiency causes the oxidation of a series of coenzymes, such as nicotinamide and flavin adenine dinucleotide, and the reduction in oxygen molecules to water molecules (H2O). Persistent deficiency has been believed to cause a loss of biological functions, even resulting in death. This classical view of oxygen has been completely revised over the last 20 years. Mammals do not have a mechanism for biosynthesizing oxygen in their bodies. In higher organisms such as vertebrates, which possess many organs, oxygen in the body is always “scarce,”; therefore, the dominant view is that organisms have evolved mechanisms to respond to the lack of this essential molecule (hypoxia), and actively use it to maintain bodily integrity. Anatomically complex, higher multicellular organisms are equipped with specialized mechanisms to enable all cells to obtain sufficient oxygen. The respiratory system consists of lungs, which provide oxygen to be transferred to hemoglobin in red blood cells, the diaphragm, other respiratory support muscles, and neuroepithelial cells that sense the partial pressure of oxygen. The cardiovascular system consists of red blood cells, an oxygen-carrying medium, the heart, the transport engine, blood vessels, and transport channels. The proper development and preservation of these systems requires the harmonious expression of thousands of genes. The transcription factor responsible for this gene expression is hypoxia-inducible factor 1 (HIF-1). In this Special Issue, we invited research and review papers on various areas of oxygen biology research that focused on the fundamental understanding of HIF signaling pathways and related gene expression profiling, as well as pharmacogenomic biomarkers, molecular targets driving the regulation of human physiology and pathophysiology, and validation in animal models. We have published six original papers and three review articles in this Special Issue. We hope that this Special Issue will reflect the current exciting research concerning HIFs and their applications in medicine and health science.
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spelling doab-20.500.12854ir-787472024-03-31T13:09:53Z Hypoxia-Inducible Factors Hirota, Kiichi hypoxia transcriptome RNA-seq ChIP-seq public database meta-analysis peripheral blood cells blood-derived therapy angiogenesis platelet rich plasma (PRP) hypoxia preconditioned plasma hypoxia preconditioned serum transcription factor hypoxia-inducible factor 1 HIF-1 hypoxia sensing acetylsalicylic acid COX-1 clopidogrel drug anticoagulation NOACs oral anticoagulation VEGF adipose-derived stem cells adipose-derived cell supension lymphangiogenesis lymphatic regeneration macrophage matrix metalloproteinase atherosclerotic plaque rupture oxidative stress xanthine oxidase HIF T cells B cells monocytes macrophages neutrophils ILC oxygen HIF-PH inhibitor gene2pubmed bibliome signature genes GPR146 enrichment analysis n/a thema EDItEUR::M Medicine and Nursing Oxygen is an essential molecule in the production of adenosine triphosphate (ATP) in cells, and a lack of energy due to O2 deficiency makes the maintenance of biological functions and human life improbable. Since oxygen functions as the final electron acceptor in the series of ATP synthesis reactions in conjunction with oxidative phosphorylation in mitochondria, its deficiency causes the oxidation of a series of coenzymes, such as nicotinamide and flavin adenine dinucleotide, and the reduction in oxygen molecules to water molecules (H2O). Persistent deficiency has been believed to cause a loss of biological functions, even resulting in death. This classical view of oxygen has been completely revised over the last 20 years. Mammals do not have a mechanism for biosynthesizing oxygen in their bodies. In higher organisms such as vertebrates, which possess many organs, oxygen in the body is always “scarce,”; therefore, the dominant view is that organisms have evolved mechanisms to respond to the lack of this essential molecule (hypoxia), and actively use it to maintain bodily integrity. Anatomically complex, higher multicellular organisms are equipped with specialized mechanisms to enable all cells to obtain sufficient oxygen. The respiratory system consists of lungs, which provide oxygen to be transferred to hemoglobin in red blood cells, the diaphragm, other respiratory support muscles, and neuroepithelial cells that sense the partial pressure of oxygen. The cardiovascular system consists of red blood cells, an oxygen-carrying medium, the heart, the transport engine, blood vessels, and transport channels. The proper development and preservation of these systems requires the harmonious expression of thousands of genes. The transcription factor responsible for this gene expression is hypoxia-inducible factor 1 (HIF-1). In this Special Issue, we invited research and review papers on various areas of oxygen biology research that focused on the fundamental understanding of HIF signaling pathways and related gene expression profiling, as well as pharmacogenomic biomarkers, molecular targets driving the regulation of human physiology and pathophysiology, and validation in animal models. We have published six original papers and three review articles in this Special Issue. We hope that this Special Issue will reflect the current exciting research concerning HIFs and their applications in medicine and health science. 2022-02-24T10:35:10Z 2022-02-24T10:35:10Z 2022 book ONIX_20220224_9783036529134_45 9783036529134 9783036529127 https://directory.doabooks.org/handle/20.500.12854/78747 eng image/jpeg Attribution 4.0 International https://mdpi.com/books/pdfview/book/4839 https://mdpi.com/books/pdfview/book/4839 MDPI - Multidisciplinary Digital Publishing Institute 10.3390/books978-3-0365-2913-4 10.3390/books978-3-0365-2913-4 46cabcaa-dd94-4bfe-87b4-55023c1b36d0 9783036529134 9783036529127 200 Basel open access
spellingShingle hypoxia
transcriptome
RNA-seq
ChIP-seq
public database
meta-analysis
peripheral blood cells
blood-derived therapy
angiogenesis
platelet rich plasma (PRP)
hypoxia preconditioned plasma
hypoxia preconditioned serum
transcription factor
hypoxia-inducible factor 1
HIF-1
hypoxia sensing
acetylsalicylic acid
COX-1
clopidogrel
drug anticoagulation
NOACs
oral anticoagulation
VEGF
adipose-derived stem cells
adipose-derived cell supension
lymphangiogenesis
lymphatic regeneration
macrophage
matrix metalloproteinase
atherosclerotic plaque rupture
oxidative stress
xanthine oxidase
HIF
T cells
B cells
monocytes
macrophages
neutrophils
ILC
oxygen
HIF-PH inhibitor
gene2pubmed
bibliome
signature genes
GPR146
enrichment analysis
n/a
thema EDItEUR::M Medicine and Nursing
Hypoxia-Inducible Factors
title Hypoxia-Inducible Factors
title_full Hypoxia-Inducible Factors
title_fullStr Hypoxia-Inducible Factors
title_full_unstemmed Hypoxia-Inducible Factors
title_short Hypoxia-Inducible Factors
title_sort hypoxia inducible factors
topic hypoxia
transcriptome
RNA-seq
ChIP-seq
public database
meta-analysis
peripheral blood cells
blood-derived therapy
angiogenesis
platelet rich plasma (PRP)
hypoxia preconditioned plasma
hypoxia preconditioned serum
transcription factor
hypoxia-inducible factor 1
HIF-1
hypoxia sensing
acetylsalicylic acid
COX-1
clopidogrel
drug anticoagulation
NOACs
oral anticoagulation
VEGF
adipose-derived stem cells
adipose-derived cell supension
lymphangiogenesis
lymphatic regeneration
macrophage
matrix metalloproteinase
atherosclerotic plaque rupture
oxidative stress
xanthine oxidase
HIF
T cells
B cells
monocytes
macrophages
neutrophils
ILC
oxygen
HIF-PH inhibitor
gene2pubmed
bibliome
signature genes
GPR146
enrichment analysis
n/a
thema EDItEUR::M Medicine and Nursing
topic_facet hypoxia
transcriptome
RNA-seq
ChIP-seq
public database
meta-analysis
peripheral blood cells
blood-derived therapy
angiogenesis
platelet rich plasma (PRP)
hypoxia preconditioned plasma
hypoxia preconditioned serum
transcription factor
hypoxia-inducible factor 1
HIF-1
hypoxia sensing
acetylsalicylic acid
COX-1
clopidogrel
drug anticoagulation
NOACs
oral anticoagulation
VEGF
adipose-derived stem cells
adipose-derived cell supension
lymphangiogenesis
lymphatic regeneration
macrophage
matrix metalloproteinase
atherosclerotic plaque rupture
oxidative stress
xanthine oxidase
HIF
T cells
B cells
monocytes
macrophages
neutrophils
ILC
oxygen
HIF-PH inhibitor
gene2pubmed
bibliome
signature genes
GPR146
enrichment analysis
n/a
thema EDItEUR::M Medicine and Nursing
url ONIX_20220224_9783036529134_45