The acute phase protein alpha-1-antitrypsin inhibits transferrin uptake in PLC/PRF/5 cells and increases release of hepatitis B virus surface antigen and alpha-fetoprotein

Propst, A; Graziadei, Ivo; Herold, M; Propst, Theresa; Vogel, Wolfgang

doi:10.1097/00042737-199806000-00011

Cited by 3 publications

(5 citation statements)

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“…In 1983, a study with 44 HBV patients found that higher levels of serum ferritin before HBV infection increased the likelihood that the infection will be persistent, [27] suggesting that iron may promote HBV infection. Other studies using cell models also found that iron promotes HBsAg release, [10] mRNA and DNA expression, [11] and HBV DNA secretion. [28] In this case, HBsAg result became negative after iron chelation therapy, along with decreased iron load.…”

Section: Discussionmentioning

confidence: 95%

“…However, some other studies using cell models found that iron inhibits HBV replication [28] and release. [10,13] Those disputable results may be due to different methods. Besides, whether these results from in vitro research could be suggestive to understand the effect of iron on HBV in human body is questionable.…”

Section: Discussionmentioning

confidence: 99%

“…Many studies have explored the connection between iron overload and HBV lifecycle with differing results. Some found that iron promotes HBV lifecycle, [10,11] whereas others found the opposite results. [12,13] In addition, the evidence on the effect of iron chelation treatment on patients with CHB with iron overload is limited.…”

Section: Introductionmentioning

confidence: 99%

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Improvement of chronic hepatitis B by iron chelation therapy in a patient with iron overload

Zou

Rong²,

Su³

et al. 2017

Medicine

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

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Improvement of chronic hepatitis B by iron chelation therapy in a patient with iron overload

Zou

Rong²,

Su³

et al. 2017

Medicine

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“…Consistent with this possibility, the endogenous acute-phase reactant and serine protease inhibitor (serpin), a-1-antitrypsin-the genetic deficiency of which predisposes to hepatocellular carcinomainhibits growth of HBV-infected liver cells (52).…”

Section: The Promise Of Proteasesmentioning

confidence: 96%

Reversing Hepatocellular Carcinoma Progression by Using Networked Biological Therapies

Epstein

Leung²

2007

Clinical Cancer Research

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The liver is distinguished from other tissues by (a) its detoxifying function, (b) its resistance to apoptosis, and (c) its regenerative response to damage. Hepatocellular carcinoma arises when chronic insults, such as hepatitis or iron overload, constitutively activate this regenerative program. Here, we propose that the proliferative response of the liver to damage underlies the resistance of hepatocellular carcinoma to cytotoxic therapy, and that hepatocellular carcinoma growth should therefore be more readily controlled by using a networked combination of noncytotoxic interventions to interrupt the damage-inducible regenerative pathway. To this end, hepatocellular carcinoma boasts a wealth of potential drug targets, including viral replication, the antiapoptotic immunosuppressant a-fetoprotein, hepatic iron overload, inflammatory signaling, extracellular proteases, and growth factors. By blocking these positive feedback loops in parallel, and so returning the host environment to a more normal state, epigenetic repression of tumor-suppressor gene function may be reversed and tumor dormancy restored. Noncytotoxic maneuvers that short circuit damage resistance loops may thus represent an indirect form of gene therapy meriting incorporation into hepatocellular carcinoma clinical trials.

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“…Many studies have explored the relationship between iron overload and the life cycle of HBV, and different results have been obtained. Some people have found that iron promotes the life cycle of HBV, [31,32] while others have found that iron limits the life cycle of HBV. [33] In 1983, a study of 44 HBV patients [34] found that higher levels of serum ferritin before HBV infection increased the likelihood of persistent infection, suggesting that iron may promote HBV infection.…”

Section: Iron Overload and Liver Diseasementioning

confidence: 99%

Relationship between iron overload caused by abnormal hepcidin expression and liver disease: A review

et al. 2023

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Iron is essential to organisms, the liver plays a vital role in its storage. Under pathological conditions, iron uptake by the intestine or hepatocytes increases, allowing excess iron to accumulate in liver cells. When the expression of hepcidin is abnormal, iron homeostasis in humans cannot be regulated, and resulting in iron overload. Hepcidin also regulates the release of iron from siderophores, thereby regulating the concentration of iron in plasma. Important factors related to hepcidin and systemic iron homeostasis include plasma iron concentration, body iron storage, infection, inflammation, and erythropoietin. This review summarizes the mechanism and regulation of iron overload caused by hepcidin, as well as related liver diseases caused by iron overload and treatment.

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The acute phase protein alpha-1-antitrypsin inhibits transferrin uptake in PLC/PRF/5 cells and increases release of hepatitis B virus surface antigen and alpha-fetoprotein

Cited by 3 publications

References 0 publications

Improvement of chronic hepatitis B by iron chelation therapy in a patient with iron overload

Improvement of chronic hepatitis B by iron chelation therapy in a patient with iron overload

Reversing Hepatocellular Carcinoma Progression by Using Networked Biological Therapies

Relationship between iron overload caused by abnormal hepcidin expression and liver disease: A review

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