Role of Zinc in Liver Pathology

AbstractSchistosomiasis is a prevalent parasitic disease worldwide. The main pathological changes of hepatosplenic schistosomiasis are hepatic granuloma and fibrosis due to worm eggs. Portal hypertension and ascites induced by hepatic fibrosis are usually the main causes of death in patients with chronic hepatosplenic schistosomiasis. Currently, no effective vaccine exists for preventing schistosome infections. For quite a long time, praziquantel (PZQ) was widely used for the treatment of schistosomiasis and has shown benefit in treating liver fibrosis. However, drug resistance and chemical toxicity from PZQ are being increasingly reported in recent years; therefore, new and effective strategies for treating schistosomiasis-induced hepatic fibrosis are urgently needed. MicroRNA (miRNA), a non-coding RNA, has been proved to be associated with the development of many human diseases, including schistosomiasis. In this review, we present a balanced and comprehensive view of the role of miRNAs in the pathogenesis, grading, and treatment of schistosomiasis-associated hepatic fibrosis. The multiple regulatory roles of miRNAs, such as promoting or inhibiting the development of liver pathology in murine schistosomiasis are also discussed in depth. Additionally, miRNAs may serve as candidate biomarkers for diagnosing liver pathology of schistosomiasis and as novel therapeutic targets for treating schistosomiasis-associated hepatic fibrosis.

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The difference in liver pathology between sporadic and familial forms of porphyria cutanea tarda: the role of iron

Journal of Hepatology ◽

10.1016/s0168-8278(95)80004-2 ◽

1995 ◽

Vol 23 (3) ◽

pp. 259-267 ◽

Cited By ~ 35

Author(s):

Peter D. Siersema ◽

Louk H.P.M. Rademakers ◽

Maud L. Cleton ◽

Fiebo J.W. ten Kate ◽

Wim C. de Bruijn ◽

...

Keyword(s):

Porphyria Cutanea Tarda ◽

Liver Pathology ◽

The Difference

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The Role of Experimental Maternal Liver Pathology in the Development of Physiological Immaturity in the Offspring

Bulletin of Experimental Biology and Medicine ◽

10.1007/s10517-013-2006-7 ◽

2013 ◽

Vol 154 (5) ◽

pp. 591-593 ◽

Cited By ~ 3

Author(s):

G. V. Bryukhin ◽

M. L. Sizonenko

Keyword(s):

Liver Pathology ◽

Maternal Liver

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Role of vasculoendothelial growth factor and its gene in pathogenesis of hepatobiliary pathology

Perm Medical Journal ◽

10.17816/pmj37436-45 ◽

2020 ◽

Vol 37 (4) ◽

pp. 36-45

Author(s):

A. P. Schekotova ◽

I. A. Bulatova

Keyword(s):

Growth Factor ◽

Liver Tumors ◽

Liver Lesion ◽

Load Level ◽

Focal Liver Lesions ◽

Liver Pathology ◽

Liver Lesions ◽

Vegf Gene ◽

Its Gene

Objective. To assess the pathogenetic value of vasculoendothelial growth factor (VEGF) and polymorphism of its gene in hepatobiliary pathology. Materials and methods. The study included 190 patients with hepatobiliary pathology (HBP): 100 patients with chronic hepatitis C (CHC) in the reactivation phase, 50 with HC in the outcome of CHC, 30 with cholelithiasis, 10 with focal liver lesions (including 8 with primary and secondary liver tumors). Results. In case of hepatobiliary pathology, VEGF, as indicator neoangiogenesis and endothelial dysfunction (ED), is a marker of the severity of liver lesion: its production is increased in some patients with cholelithiasis, moderately elevated in all patients with CH and significantly elevated against the background of HC and liver pathology of the tumor genesis. In chronic diffuse diseases of the liver, there are detected multiple reliable relationships between VEGF and a number of ED indices, hepatic clinical and biochemical syndromes, liver fibrosis markers, viral load level that proves the obligate involvement of VEGF in the development and progression of liver pathology. VEGF can be used as a test for differential diagnosis of fibrosis in CH and HC with the sensibility of 90 % and specificity of 78 %. Carriage of the allele C in the locus of the VEGF gene (G-634C) in the form of homozygote CC can show the risk of more severe lesion of the liver in CHC and is interconnected with increased production of VEGF. Conclusions. Vasculoendothelial growth factor and polymorphism of its gene is involved in the pathogenesis of hepatobiliary pathology, activating neoangiogenesis and fibrosis in the liver.

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Effects of Alcohol and Oxidative Stress on Liver Pathology: The Role of the Mitochondrion

Alcoholism Clinical and Experimental Research ◽

10.1111/j.1530-0277.2002.tb02621.x ◽

2002 ◽

Vol 26 (6) ◽

pp. 907-915 ◽

Cited By ~ 97

Author(s):

Alan Cahill ◽

Carol C. Cunningham ◽

Masayuki Adachi ◽

Hiromasa Ishii ◽

Shannon M. Bailey ◽

...

Keyword(s):

Oxidative Stress ◽

Liver Pathology ◽

And Oxidative Stress

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Role of peroxisome proliferator-activated receptors in the control of alcohol dependence and concomitant liver pathology

Proceedings of the National Academy of Sciences of Belarus Medical series ◽

10.29235/1814-6023-2019-16-2-244-256 ◽

2019 ◽

Vol 16 (2) ◽

pp. 244-256

Author(s):

I. N. Semenenya ◽

A. H. Shlyahtun ◽

H. F. Raduta

Keyword(s):

Liver Disease ◽

Alcohol Dependence ◽

Alcoholic Liver Disease ◽

Therapeutic Potential ◽

Scattered Data ◽

Peroxisome Proliferator ◽

Liver Pathology ◽

Ppar Agonists ◽

Peroxisome Proliferator Activated Receptors

The article is aimed to summarize the scattered data on the role of peroxisome proliferator-activated receptors (PPAR) and the possibility of using PPAR’s agonists for treatment of alcohol dependence and alcoholic liver disease. Earlier it was shown that some PPAR agonists can reduce ethanol consumption and preference in rodents. Several hypotheses considering the antialcoholic activity of PPAR agonists and the roles of PPAR in the development of alcohol dependence were discussed. In light of these data, the therapeutic potential of PPARs agonists as an agent for the treatment of alcoholism, has been reviewed.

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AAV-HDV: An Attractive Platform for the In Vivo Study of HDV Biology and the Mechanism of Disease Pathogenesis

Viruses ◽

10.3390/v13050788 ◽

2021 ◽

Vol 13 (5) ◽

pp. 788

Author(s):

Sheila Maestro ◽

Nahia Gómez-Echarte ◽

Gracián Camps ◽

Carla Usai ◽

Lester Suárez ◽

...

Keyword(s):

Liver Damage ◽

Molecular Mechanisms ◽

Severe Form ◽

Liver Pathology ◽

Early Expression ◽

Hdv Infection ◽

Viral Components

Hepatitis delta virus (HDV) infection causes the most severe form of viral hepatitis, but little is known about the molecular mechanisms involved. We have recently developed an HDV mouse model based on the delivery of HDV replication-competent genomes using adeno-associated vectors (AAV), which developed a liver pathology very similar to the human disease and allowed us to perform mechanistic studies. We have generated different AAV-HDV mutants to eliminate the expression of HDV antigens (HDAgs), and we have characterized them both in vitro and in vivo. We confirmed that S-HDAg is essential for HDV replication and cannot be replaced by L-HDAg or host cellular proteins, and that L-HDAg is essential to produce the HDV infectious particle and inhibits its replication. We have also found that lack of L-HDAg resulted in the increase of S-HDAg expression levels and the exacerbation of liver damage, which was associated with an increment in liver inflammation but did not require T cells. Interestingly, early expression of L-HDAg significantly ameliorated the liver damage induced by the mutant expressing only S-HDAg. In summary, the use of AAV-HDV represents a very attractive platform to interrogate in vivo the role of viral components in the HDV life cycle and to better understand the mechanism of HDV-induced liver pathology.

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