Hypoxia. The role of hypoxia and HIF-dependent signalling events in rheumatoid arthritis
Abstract An adequate supply of oxygen and nutrients is essential for survival and metabolism of cells, and consequentially for normal homeostasis. Alterations in tissue oxygen tension have been postulated to contribute to a number of pathologies, including rheumatoid arthritis (RA), in which the cha...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Muz, Barbara [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2009 |
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| Schlagwörter: |
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| Anmerkung: |
© BioMed Central Ltd 2009 |
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| Übergeordnetes Werk: |
Enthalten in: Arthritis Research & Therapy - London : BioMed Central, 1999, 11(2009), 1 vom: 20. Jan. |
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| Übergeordnetes Werk: |
volume:11 ; year:2009 ; number:1 ; day:20 ; month:01 |
| Links: |
|---|
| DOI / URN: |
10.1186/ar2568 |
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| Katalog-ID: |
SPR030829666 |
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| 520 | |a Abstract An adequate supply of oxygen and nutrients is essential for survival and metabolism of cells, and consequentially for normal homeostasis. Alterations in tissue oxygen tension have been postulated to contribute to a number of pathologies, including rheumatoid arthritis (RA), in which the characteristic synovial expansion is thought to outstrip the oxygen supply, leading to areas of synovial hypoxia and hypoperfusion. Indeed, the idea of a therapeutic modality aimed at 'starving' tissue of blood vessels was born from the concept that blood vessel formation (angiogenesis) is central to efficient delivery of oxygen to cells and tissues, and has underpinned the development of anti-angiogenic therapies for a range of cancers. An important and well characterized 'master regulator' of the adaptive response to alterations in oxygen tension is hypoxia-inducible factor (HIF), which is exquisitely sensitive to changes in oxygen tension. Activation of the HIF transcription factor signalling cascade leads to extensive changes in gene expression, which allow cells, tissues and organisms to adapt to reduced oxygenation. One of the best characterized hypoxia-responsive genes is the angiogenic stimulus vascular endothelial growth factor, expression of which is dramatically upregulated by hypoxia in many cells types, including RA synovial membrane cells. This leads to an apparent paradox, with the abundant synovial vasculature (which might be expected to restore oxygen levels to normal) occurring nonetheless together with regions of synovial hypoxia. It has been shown in a number of studies that vascular endothelial growth factor blockade is effective in animal models of arthritis; these findings suggest that hypoxia may activate the angiogenic cascade, thereby contributing to RA development. Recent data also suggest that, as well as activating angiogenesis, hypoxia may regulate many other features that are important in RA, such as cell trafficking and matrix degradation. An understanding of the biology of the HIF transcription family may eventually lead to the development of therapies that are aimed at interfering with this key signalling pathway, and hence to modulation of hypoxia-dependent pathologies such as RA. | ||
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10.1186/ar2568 doi (DE-627)SPR030829666 (SPR)ar2568-e DE-627 ger DE-627 rakwb eng Muz, Barbara verfasserin aut Hypoxia. The role of hypoxia and HIF-dependent signalling events in rheumatoid arthritis 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2009 Abstract An adequate supply of oxygen and nutrients is essential for survival and metabolism of cells, and consequentially for normal homeostasis. Alterations in tissue oxygen tension have been postulated to contribute to a number of pathologies, including rheumatoid arthritis (RA), in which the characteristic synovial expansion is thought to outstrip the oxygen supply, leading to areas of synovial hypoxia and hypoperfusion. Indeed, the idea of a therapeutic modality aimed at 'starving' tissue of blood vessels was born from the concept that blood vessel formation (angiogenesis) is central to efficient delivery of oxygen to cells and tissues, and has underpinned the development of anti-angiogenic therapies for a range of cancers. An important and well characterized 'master regulator' of the adaptive response to alterations in oxygen tension is hypoxia-inducible factor (HIF), which is exquisitely sensitive to changes in oxygen tension. Activation of the HIF transcription factor signalling cascade leads to extensive changes in gene expression, which allow cells, tissues and organisms to adapt to reduced oxygenation. One of the best characterized hypoxia-responsive genes is the angiogenic stimulus vascular endothelial growth factor, expression of which is dramatically upregulated by hypoxia in many cells types, including RA synovial membrane cells. This leads to an apparent paradox, with the abundant synovial vasculature (which might be expected to restore oxygen levels to normal) occurring nonetheless together with regions of synovial hypoxia. It has been shown in a number of studies that vascular endothelial growth factor blockade is effective in animal models of arthritis; these findings suggest that hypoxia may activate the angiogenic cascade, thereby contributing to RA development. Recent data also suggest that, as well as activating angiogenesis, hypoxia may regulate many other features that are important in RA, such as cell trafficking and matrix degradation. An understanding of the biology of the HIF transcription family may eventually lead to the development of therapies that are aimed at interfering with this key signalling pathway, and hence to modulation of hypoxia-dependent pathologies such as RA. Rheumatoid Arthritis (dpeaa)DE-He213 Rheumatoid Arthritis Patient (dpeaa)DE-He213 Rheumatoid Arthritis Synovium (dpeaa)DE-He213 Rheumatoid Arthritis Synovial Fibroblast (dpeaa)DE-He213 Hypoxia Tolerance (dpeaa)DE-He213 Khan, Moddasar N aut Kiriakidis, Serafim aut Paleolog, Ewa M aut Enthalten in Arthritis Research & Therapy London : BioMed Central, 1999 11(2009), 1 vom: 20. Jan. (DE-627)326646418 (DE-600)2041668-4 1478-6354 nnns volume:11 year:2009 number:1 day:20 month:01 https://dx.doi.org/10.1186/ar2568 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2009 1 20 01 |
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10.1186/ar2568 doi (DE-627)SPR030829666 (SPR)ar2568-e DE-627 ger DE-627 rakwb eng Muz, Barbara verfasserin aut Hypoxia. The role of hypoxia and HIF-dependent signalling events in rheumatoid arthritis 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2009 Abstract An adequate supply of oxygen and nutrients is essential for survival and metabolism of cells, and consequentially for normal homeostasis. Alterations in tissue oxygen tension have been postulated to contribute to a number of pathologies, including rheumatoid arthritis (RA), in which the characteristic synovial expansion is thought to outstrip the oxygen supply, leading to areas of synovial hypoxia and hypoperfusion. Indeed, the idea of a therapeutic modality aimed at 'starving' tissue of blood vessels was born from the concept that blood vessel formation (angiogenesis) is central to efficient delivery of oxygen to cells and tissues, and has underpinned the development of anti-angiogenic therapies for a range of cancers. An important and well characterized 'master regulator' of the adaptive response to alterations in oxygen tension is hypoxia-inducible factor (HIF), which is exquisitely sensitive to changes in oxygen tension. Activation of the HIF transcription factor signalling cascade leads to extensive changes in gene expression, which allow cells, tissues and organisms to adapt to reduced oxygenation. One of the best characterized hypoxia-responsive genes is the angiogenic stimulus vascular endothelial growth factor, expression of which is dramatically upregulated by hypoxia in many cells types, including RA synovial membrane cells. This leads to an apparent paradox, with the abundant synovial vasculature (which might be expected to restore oxygen levels to normal) occurring nonetheless together with regions of synovial hypoxia. It has been shown in a number of studies that vascular endothelial growth factor blockade is effective in animal models of arthritis; these findings suggest that hypoxia may activate the angiogenic cascade, thereby contributing to RA development. Recent data also suggest that, as well as activating angiogenesis, hypoxia may regulate many other features that are important in RA, such as cell trafficking and matrix degradation. An understanding of the biology of the HIF transcription family may eventually lead to the development of therapies that are aimed at interfering with this key signalling pathway, and hence to modulation of hypoxia-dependent pathologies such as RA. Rheumatoid Arthritis (dpeaa)DE-He213 Rheumatoid Arthritis Patient (dpeaa)DE-He213 Rheumatoid Arthritis Synovium (dpeaa)DE-He213 Rheumatoid Arthritis Synovial Fibroblast (dpeaa)DE-He213 Hypoxia Tolerance (dpeaa)DE-He213 Khan, Moddasar N aut Kiriakidis, Serafim aut Paleolog, Ewa M aut Enthalten in Arthritis Research & Therapy London : BioMed Central, 1999 11(2009), 1 vom: 20. Jan. (DE-627)326646418 (DE-600)2041668-4 1478-6354 nnns volume:11 year:2009 number:1 day:20 month:01 https://dx.doi.org/10.1186/ar2568 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2009 1 20 01 |
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10.1186/ar2568 doi (DE-627)SPR030829666 (SPR)ar2568-e DE-627 ger DE-627 rakwb eng Muz, Barbara verfasserin aut Hypoxia. The role of hypoxia and HIF-dependent signalling events in rheumatoid arthritis 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2009 Abstract An adequate supply of oxygen and nutrients is essential for survival and metabolism of cells, and consequentially for normal homeostasis. Alterations in tissue oxygen tension have been postulated to contribute to a number of pathologies, including rheumatoid arthritis (RA), in which the characteristic synovial expansion is thought to outstrip the oxygen supply, leading to areas of synovial hypoxia and hypoperfusion. Indeed, the idea of a therapeutic modality aimed at 'starving' tissue of blood vessels was born from the concept that blood vessel formation (angiogenesis) is central to efficient delivery of oxygen to cells and tissues, and has underpinned the development of anti-angiogenic therapies for a range of cancers. An important and well characterized 'master regulator' of the adaptive response to alterations in oxygen tension is hypoxia-inducible factor (HIF), which is exquisitely sensitive to changes in oxygen tension. Activation of the HIF transcription factor signalling cascade leads to extensive changes in gene expression, which allow cells, tissues and organisms to adapt to reduced oxygenation. One of the best characterized hypoxia-responsive genes is the angiogenic stimulus vascular endothelial growth factor, expression of which is dramatically upregulated by hypoxia in many cells types, including RA synovial membrane cells. This leads to an apparent paradox, with the abundant synovial vasculature (which might be expected to restore oxygen levels to normal) occurring nonetheless together with regions of synovial hypoxia. It has been shown in a number of studies that vascular endothelial growth factor blockade is effective in animal models of arthritis; these findings suggest that hypoxia may activate the angiogenic cascade, thereby contributing to RA development. Recent data also suggest that, as well as activating angiogenesis, hypoxia may regulate many other features that are important in RA, such as cell trafficking and matrix degradation. An understanding of the biology of the HIF transcription family may eventually lead to the development of therapies that are aimed at interfering with this key signalling pathway, and hence to modulation of hypoxia-dependent pathologies such as RA. Rheumatoid Arthritis (dpeaa)DE-He213 Rheumatoid Arthritis Patient (dpeaa)DE-He213 Rheumatoid Arthritis Synovium (dpeaa)DE-He213 Rheumatoid Arthritis Synovial Fibroblast (dpeaa)DE-He213 Hypoxia Tolerance (dpeaa)DE-He213 Khan, Moddasar N aut Kiriakidis, Serafim aut Paleolog, Ewa M aut Enthalten in Arthritis Research & Therapy London : BioMed Central, 1999 11(2009), 1 vom: 20. Jan. (DE-627)326646418 (DE-600)2041668-4 1478-6354 nnns volume:11 year:2009 number:1 day:20 month:01 https://dx.doi.org/10.1186/ar2568 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2009 1 20 01 |
| allfieldsGer |
10.1186/ar2568 doi (DE-627)SPR030829666 (SPR)ar2568-e DE-627 ger DE-627 rakwb eng Muz, Barbara verfasserin aut Hypoxia. The role of hypoxia and HIF-dependent signalling events in rheumatoid arthritis 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2009 Abstract An adequate supply of oxygen and nutrients is essential for survival and metabolism of cells, and consequentially for normal homeostasis. Alterations in tissue oxygen tension have been postulated to contribute to a number of pathologies, including rheumatoid arthritis (RA), in which the characteristic synovial expansion is thought to outstrip the oxygen supply, leading to areas of synovial hypoxia and hypoperfusion. Indeed, the idea of a therapeutic modality aimed at 'starving' tissue of blood vessels was born from the concept that blood vessel formation (angiogenesis) is central to efficient delivery of oxygen to cells and tissues, and has underpinned the development of anti-angiogenic therapies for a range of cancers. An important and well characterized 'master regulator' of the adaptive response to alterations in oxygen tension is hypoxia-inducible factor (HIF), which is exquisitely sensitive to changes in oxygen tension. Activation of the HIF transcription factor signalling cascade leads to extensive changes in gene expression, which allow cells, tissues and organisms to adapt to reduced oxygenation. One of the best characterized hypoxia-responsive genes is the angiogenic stimulus vascular endothelial growth factor, expression of which is dramatically upregulated by hypoxia in many cells types, including RA synovial membrane cells. This leads to an apparent paradox, with the abundant synovial vasculature (which might be expected to restore oxygen levels to normal) occurring nonetheless together with regions of synovial hypoxia. It has been shown in a number of studies that vascular endothelial growth factor blockade is effective in animal models of arthritis; these findings suggest that hypoxia may activate the angiogenic cascade, thereby contributing to RA development. Recent data also suggest that, as well as activating angiogenesis, hypoxia may regulate many other features that are important in RA, such as cell trafficking and matrix degradation. An understanding of the biology of the HIF transcription family may eventually lead to the development of therapies that are aimed at interfering with this key signalling pathway, and hence to modulation of hypoxia-dependent pathologies such as RA. Rheumatoid Arthritis (dpeaa)DE-He213 Rheumatoid Arthritis Patient (dpeaa)DE-He213 Rheumatoid Arthritis Synovium (dpeaa)DE-He213 Rheumatoid Arthritis Synovial Fibroblast (dpeaa)DE-He213 Hypoxia Tolerance (dpeaa)DE-He213 Khan, Moddasar N aut Kiriakidis, Serafim aut Paleolog, Ewa M aut Enthalten in Arthritis Research & Therapy London : BioMed Central, 1999 11(2009), 1 vom: 20. Jan. (DE-627)326646418 (DE-600)2041668-4 1478-6354 nnns volume:11 year:2009 number:1 day:20 month:01 https://dx.doi.org/10.1186/ar2568 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2009 1 20 01 |
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10.1186/ar2568 doi (DE-627)SPR030829666 (SPR)ar2568-e DE-627 ger DE-627 rakwb eng Muz, Barbara verfasserin aut Hypoxia. The role of hypoxia and HIF-dependent signalling events in rheumatoid arthritis 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2009 Abstract An adequate supply of oxygen and nutrients is essential for survival and metabolism of cells, and consequentially for normal homeostasis. Alterations in tissue oxygen tension have been postulated to contribute to a number of pathologies, including rheumatoid arthritis (RA), in which the characteristic synovial expansion is thought to outstrip the oxygen supply, leading to areas of synovial hypoxia and hypoperfusion. Indeed, the idea of a therapeutic modality aimed at 'starving' tissue of blood vessels was born from the concept that blood vessel formation (angiogenesis) is central to efficient delivery of oxygen to cells and tissues, and has underpinned the development of anti-angiogenic therapies for a range of cancers. An important and well characterized 'master regulator' of the adaptive response to alterations in oxygen tension is hypoxia-inducible factor (HIF), which is exquisitely sensitive to changes in oxygen tension. Activation of the HIF transcription factor signalling cascade leads to extensive changes in gene expression, which allow cells, tissues and organisms to adapt to reduced oxygenation. One of the best characterized hypoxia-responsive genes is the angiogenic stimulus vascular endothelial growth factor, expression of which is dramatically upregulated by hypoxia in many cells types, including RA synovial membrane cells. This leads to an apparent paradox, with the abundant synovial vasculature (which might be expected to restore oxygen levels to normal) occurring nonetheless together with regions of synovial hypoxia. It has been shown in a number of studies that vascular endothelial growth factor blockade is effective in animal models of arthritis; these findings suggest that hypoxia may activate the angiogenic cascade, thereby contributing to RA development. Recent data also suggest that, as well as activating angiogenesis, hypoxia may regulate many other features that are important in RA, such as cell trafficking and matrix degradation. An understanding of the biology of the HIF transcription family may eventually lead to the development of therapies that are aimed at interfering with this key signalling pathway, and hence to modulation of hypoxia-dependent pathologies such as RA. Rheumatoid Arthritis (dpeaa)DE-He213 Rheumatoid Arthritis Patient (dpeaa)DE-He213 Rheumatoid Arthritis Synovium (dpeaa)DE-He213 Rheumatoid Arthritis Synovial Fibroblast (dpeaa)DE-He213 Hypoxia Tolerance (dpeaa)DE-He213 Khan, Moddasar N aut Kiriakidis, Serafim aut Paleolog, Ewa M aut Enthalten in Arthritis Research & Therapy London : BioMed Central, 1999 11(2009), 1 vom: 20. Jan. (DE-627)326646418 (DE-600)2041668-4 1478-6354 nnns volume:11 year:2009 number:1 day:20 month:01 https://dx.doi.org/10.1186/ar2568 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 11 2009 1 20 01 |
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Hypoxia. The role of hypoxia and HIF-dependent signalling events in rheumatoid arthritis |
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Abstract An adequate supply of oxygen and nutrients is essential for survival and metabolism of cells, and consequentially for normal homeostasis. Alterations in tissue oxygen tension have been postulated to contribute to a number of pathologies, including rheumatoid arthritis (RA), in which the characteristic synovial expansion is thought to outstrip the oxygen supply, leading to areas of synovial hypoxia and hypoperfusion. Indeed, the idea of a therapeutic modality aimed at 'starving' tissue of blood vessels was born from the concept that blood vessel formation (angiogenesis) is central to efficient delivery of oxygen to cells and tissues, and has underpinned the development of anti-angiogenic therapies for a range of cancers. An important and well characterized 'master regulator' of the adaptive response to alterations in oxygen tension is hypoxia-inducible factor (HIF), which is exquisitely sensitive to changes in oxygen tension. Activation of the HIF transcription factor signalling cascade leads to extensive changes in gene expression, which allow cells, tissues and organisms to adapt to reduced oxygenation. One of the best characterized hypoxia-responsive genes is the angiogenic stimulus vascular endothelial growth factor, expression of which is dramatically upregulated by hypoxia in many cells types, including RA synovial membrane cells. This leads to an apparent paradox, with the abundant synovial vasculature (which might be expected to restore oxygen levels to normal) occurring nonetheless together with regions of synovial hypoxia. It has been shown in a number of studies that vascular endothelial growth factor blockade is effective in animal models of arthritis; these findings suggest that hypoxia may activate the angiogenic cascade, thereby contributing to RA development. Recent data also suggest that, as well as activating angiogenesis, hypoxia may regulate many other features that are important in RA, such as cell trafficking and matrix degradation. An understanding of the biology of the HIF transcription family may eventually lead to the development of therapies that are aimed at interfering with this key signalling pathway, and hence to modulation of hypoxia-dependent pathologies such as RA. © BioMed Central Ltd 2009 |
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Abstract An adequate supply of oxygen and nutrients is essential for survival and metabolism of cells, and consequentially for normal homeostasis. Alterations in tissue oxygen tension have been postulated to contribute to a number of pathologies, including rheumatoid arthritis (RA), in which the characteristic synovial expansion is thought to outstrip the oxygen supply, leading to areas of synovial hypoxia and hypoperfusion. Indeed, the idea of a therapeutic modality aimed at 'starving' tissue of blood vessels was born from the concept that blood vessel formation (angiogenesis) is central to efficient delivery of oxygen to cells and tissues, and has underpinned the development of anti-angiogenic therapies for a range of cancers. An important and well characterized 'master regulator' of the adaptive response to alterations in oxygen tension is hypoxia-inducible factor (HIF), which is exquisitely sensitive to changes in oxygen tension. Activation of the HIF transcription factor signalling cascade leads to extensive changes in gene expression, which allow cells, tissues and organisms to adapt to reduced oxygenation. One of the best characterized hypoxia-responsive genes is the angiogenic stimulus vascular endothelial growth factor, expression of which is dramatically upregulated by hypoxia in many cells types, including RA synovial membrane cells. This leads to an apparent paradox, with the abundant synovial vasculature (which might be expected to restore oxygen levels to normal) occurring nonetheless together with regions of synovial hypoxia. It has been shown in a number of studies that vascular endothelial growth factor blockade is effective in animal models of arthritis; these findings suggest that hypoxia may activate the angiogenic cascade, thereby contributing to RA development. Recent data also suggest that, as well as activating angiogenesis, hypoxia may regulate many other features that are important in RA, such as cell trafficking and matrix degradation. An understanding of the biology of the HIF transcription family may eventually lead to the development of therapies that are aimed at interfering with this key signalling pathway, and hence to modulation of hypoxia-dependent pathologies such as RA. © BioMed Central Ltd 2009 |
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Abstract An adequate supply of oxygen and nutrients is essential for survival and metabolism of cells, and consequentially for normal homeostasis. Alterations in tissue oxygen tension have been postulated to contribute to a number of pathologies, including rheumatoid arthritis (RA), in which the characteristic synovial expansion is thought to outstrip the oxygen supply, leading to areas of synovial hypoxia and hypoperfusion. Indeed, the idea of a therapeutic modality aimed at 'starving' tissue of blood vessels was born from the concept that blood vessel formation (angiogenesis) is central to efficient delivery of oxygen to cells and tissues, and has underpinned the development of anti-angiogenic therapies for a range of cancers. An important and well characterized 'master regulator' of the adaptive response to alterations in oxygen tension is hypoxia-inducible factor (HIF), which is exquisitely sensitive to changes in oxygen tension. Activation of the HIF transcription factor signalling cascade leads to extensive changes in gene expression, which allow cells, tissues and organisms to adapt to reduced oxygenation. One of the best characterized hypoxia-responsive genes is the angiogenic stimulus vascular endothelial growth factor, expression of which is dramatically upregulated by hypoxia in many cells types, including RA synovial membrane cells. This leads to an apparent paradox, with the abundant synovial vasculature (which might be expected to restore oxygen levels to normal) occurring nonetheless together with regions of synovial hypoxia. It has been shown in a number of studies that vascular endothelial growth factor blockade is effective in animal models of arthritis; these findings suggest that hypoxia may activate the angiogenic cascade, thereby contributing to RA development. Recent data also suggest that, as well as activating angiogenesis, hypoxia may regulate many other features that are important in RA, such as cell trafficking and matrix degradation. An understanding of the biology of the HIF transcription family may eventually lead to the development of therapies that are aimed at interfering with this key signalling pathway, and hence to modulation of hypoxia-dependent pathologies such as RA. © BioMed Central Ltd 2009 |
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One of the best characterized hypoxia-responsive genes is the angiogenic stimulus vascular endothelial growth factor, expression of which is dramatically upregulated by hypoxia in many cells types, including RA synovial membrane cells. This leads to an apparent paradox, with the abundant synovial vasculature (which might be expected to restore oxygen levels to normal) occurring nonetheless together with regions of synovial hypoxia. It has been shown in a number of studies that vascular endothelial growth factor blockade is effective in animal models of arthritis; these findings suggest that hypoxia may activate the angiogenic cascade, thereby contributing to RA development. Recent data also suggest that, as well as activating angiogenesis, hypoxia may regulate many other features that are important in RA, such as cell trafficking and matrix degradation. 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