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Hypoxia-inducible factor may induce the development of liver fibrosis in Budd–Chiari syndrome by regulating CD248/endosialin expression: A hypothesis
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Zeitschriftentitel: | Journal of Translational Internal Medicine |
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Personen und Körperschaften: | , , , , |
In: | Journal of Translational Internal Medicine, 6, 2018, 2, S. 66-69 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
Walter de Gruyter GmbH
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Schlagwörter: |
author_facet |
Tian, Ye Deng, Han Han, Lei Hu, Sijun Qi, Xingshun Tian, Ye Deng, Han Han, Lei Hu, Sijun Qi, Xingshun |
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author |
Tian, Ye Deng, Han Han, Lei Hu, Sijun Qi, Xingshun |
spellingShingle |
Tian, Ye Deng, Han Han, Lei Hu, Sijun Qi, Xingshun Journal of Translational Internal Medicine Hypoxia-inducible factor may induce the development of liver fibrosis in Budd–Chiari syndrome by regulating CD248/endosialin expression: A hypothesis Internal Medicine |
author_sort |
tian, ye |
spelling |
Tian, Ye Deng, Han Han, Lei Hu, Sijun Qi, Xingshun 2224-4018 Walter de Gruyter GmbH Internal Medicine http://dx.doi.org/10.2478/jtim-2018-0018 <jats:title>Abstract</jats:title> <jats:p>Budd-Chiari syndrome (BCS) leads to the development of liver fibrosis in most of the cases. However, the mechanism of BCS-related liver fibrosis is unclear, and it may be largely different from that induced by chronic viral hepatitis. Hepatic stellate cell (HSC) and its specific marker CD248/endosialin are known to play an important regulatory role in the development of liver fibrosis. Additionally, hypoxia microenvironment and hypoxia-inducible factor (HIF) are involved in the regulation of CD248/endosialin. Therefore, we hypothesize that hypoxia microenvironment which develops due to BCS can regulate the expression of CD248/endosialin in HSC via HIF signaling pathway, which then affects the function of HSC and development of liver fibrosis. To confirm the hypothesis, two major investigations are necessary: (1) in the BCS animal model and clinical studies, the relationship between the severity of liver fibrosis and the expression of HIF and CD248/endosialin in HSC will be explored; and (2) in the <jats:italic>in vitro</jats:italic> cell system, the effect of hypoxic microenvironment, HIF-1α or HIF-2α, on the expression of CD248/endosialin in HSC will be explored. It will be important to elucidate whether HIF signaling pathway regulates the expression of CD248/endosialin, thereby inducing the development of BCS-related liver fibrosis.</jats:p> Hypoxia-inducible factor may induce the development of liver fibrosis in Budd–Chiari syndrome by regulating CD248/endosialin expression: A hypothesis Journal of Translational Internal Medicine |
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10.2478/jtim-2018-0018 |
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title |
Hypoxia-inducible factor may induce the development of liver fibrosis in Budd–Chiari syndrome by regulating CD248/endosialin expression: A hypothesis |
title_unstemmed |
Hypoxia-inducible factor may induce the development of liver fibrosis in Budd–Chiari syndrome by regulating CD248/endosialin expression: A hypothesis |
title_full |
Hypoxia-inducible factor may induce the development of liver fibrosis in Budd–Chiari syndrome by regulating CD248/endosialin expression: A hypothesis |
title_fullStr |
Hypoxia-inducible factor may induce the development of liver fibrosis in Budd–Chiari syndrome by regulating CD248/endosialin expression: A hypothesis |
title_full_unstemmed |
Hypoxia-inducible factor may induce the development of liver fibrosis in Budd–Chiari syndrome by regulating CD248/endosialin expression: A hypothesis |
title_short |
Hypoxia-inducible factor may induce the development of liver fibrosis in Budd–Chiari syndrome by regulating CD248/endosialin expression: A hypothesis |
title_sort |
hypoxia-inducible factor may induce the development of liver fibrosis in budd–chiari syndrome by regulating cd248/endosialin expression: a hypothesis |
topic |
Internal Medicine |
url |
http://dx.doi.org/10.2478/jtim-2018-0018 |
publishDate |
2018 |
physical |
66-69 |
description |
<jats:title>Abstract</jats:title>
<jats:p>Budd-Chiari syndrome (BCS) leads to the development of liver fibrosis in most of the cases. However, the mechanism of BCS-related liver fibrosis is unclear, and it may be largely different from that induced by chronic viral hepatitis. Hepatic stellate cell (HSC) and its specific marker CD248/endosialin are known to play an important regulatory role in the development of liver fibrosis. Additionally, hypoxia microenvironment and hypoxia-inducible factor (HIF) are involved in the regulation of CD248/endosialin. Therefore, we hypothesize that hypoxia microenvironment which develops due to BCS can regulate the expression of CD248/endosialin in HSC via HIF signaling pathway, which then affects the function of HSC and development of liver fibrosis. To confirm the hypothesis, two major investigations are necessary: (1) in the BCS animal model and clinical studies, the relationship between the severity of liver fibrosis and the expression of HIF and CD248/endosialin in HSC will be explored; and (2) in the <jats:italic>in vitro</jats:italic> cell system, the effect of hypoxic microenvironment, HIF-1α or HIF-2α, on the expression of CD248/endosialin in HSC will be explored. It will be important to elucidate whether HIF signaling pathway regulates the expression of CD248/endosialin, thereby inducing the development of BCS-related liver fibrosis.</jats:p> |
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author | Tian, Ye, Deng, Han, Han, Lei, Hu, Sijun, Qi, Xingshun |
author_facet | Tian, Ye, Deng, Han, Han, Lei, Hu, Sijun, Qi, Xingshun, Tian, Ye, Deng, Han, Han, Lei, Hu, Sijun, Qi, Xingshun |
author_sort | tian, ye |
container_issue | 2 |
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container_title | Journal of Translational Internal Medicine |
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description | <jats:title>Abstract</jats:title> <jats:p>Budd-Chiari syndrome (BCS) leads to the development of liver fibrosis in most of the cases. However, the mechanism of BCS-related liver fibrosis is unclear, and it may be largely different from that induced by chronic viral hepatitis. Hepatic stellate cell (HSC) and its specific marker CD248/endosialin are known to play an important regulatory role in the development of liver fibrosis. Additionally, hypoxia microenvironment and hypoxia-inducible factor (HIF) are involved in the regulation of CD248/endosialin. Therefore, we hypothesize that hypoxia microenvironment which develops due to BCS can regulate the expression of CD248/endosialin in HSC via HIF signaling pathway, which then affects the function of HSC and development of liver fibrosis. To confirm the hypothesis, two major investigations are necessary: (1) in the BCS animal model and clinical studies, the relationship between the severity of liver fibrosis and the expression of HIF and CD248/endosialin in HSC will be explored; and (2) in the <jats:italic>in vitro</jats:italic> cell system, the effect of hypoxic microenvironment, HIF-1α or HIF-2α, on the expression of CD248/endosialin in HSC will be explored. It will be important to elucidate whether HIF signaling pathway regulates the expression of CD248/endosialin, thereby inducing the development of BCS-related liver fibrosis.</jats:p> |
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spelling | Tian, Ye Deng, Han Han, Lei Hu, Sijun Qi, Xingshun 2224-4018 Walter de Gruyter GmbH Internal Medicine http://dx.doi.org/10.2478/jtim-2018-0018 <jats:title>Abstract</jats:title> <jats:p>Budd-Chiari syndrome (BCS) leads to the development of liver fibrosis in most of the cases. However, the mechanism of BCS-related liver fibrosis is unclear, and it may be largely different from that induced by chronic viral hepatitis. Hepatic stellate cell (HSC) and its specific marker CD248/endosialin are known to play an important regulatory role in the development of liver fibrosis. Additionally, hypoxia microenvironment and hypoxia-inducible factor (HIF) are involved in the regulation of CD248/endosialin. Therefore, we hypothesize that hypoxia microenvironment which develops due to BCS can regulate the expression of CD248/endosialin in HSC via HIF signaling pathway, which then affects the function of HSC and development of liver fibrosis. To confirm the hypothesis, two major investigations are necessary: (1) in the BCS animal model and clinical studies, the relationship between the severity of liver fibrosis and the expression of HIF and CD248/endosialin in HSC will be explored; and (2) in the <jats:italic>in vitro</jats:italic> cell system, the effect of hypoxic microenvironment, HIF-1α or HIF-2α, on the expression of CD248/endosialin in HSC will be explored. It will be important to elucidate whether HIF signaling pathway regulates the expression of CD248/endosialin, thereby inducing the development of BCS-related liver fibrosis.</jats:p> Hypoxia-inducible factor may induce the development of liver fibrosis in Budd–Chiari syndrome by regulating CD248/endosialin expression: A hypothesis Journal of Translational Internal Medicine |
spellingShingle | Tian, Ye, Deng, Han, Han, Lei, Hu, Sijun, Qi, Xingshun, Journal of Translational Internal Medicine, Hypoxia-inducible factor may induce the development of liver fibrosis in Budd–Chiari syndrome by regulating CD248/endosialin expression: A hypothesis, Internal Medicine |
title | Hypoxia-inducible factor may induce the development of liver fibrosis in Budd–Chiari syndrome by regulating CD248/endosialin expression: A hypothesis |
title_full | Hypoxia-inducible factor may induce the development of liver fibrosis in Budd–Chiari syndrome by regulating CD248/endosialin expression: A hypothesis |
title_fullStr | Hypoxia-inducible factor may induce the development of liver fibrosis in Budd–Chiari syndrome by regulating CD248/endosialin expression: A hypothesis |
title_full_unstemmed | Hypoxia-inducible factor may induce the development of liver fibrosis in Budd–Chiari syndrome by regulating CD248/endosialin expression: A hypothesis |
title_short | Hypoxia-inducible factor may induce the development of liver fibrosis in Budd–Chiari syndrome by regulating CD248/endosialin expression: A hypothesis |
title_sort | hypoxia-inducible factor may induce the development of liver fibrosis in budd–chiari syndrome by regulating cd248/endosialin expression: a hypothesis |
title_unstemmed | Hypoxia-inducible factor may induce the development of liver fibrosis in Budd–Chiari syndrome by regulating CD248/endosialin expression: A hypothesis |
topic | Internal Medicine |
url | http://dx.doi.org/10.2478/jtim-2018-0018 |