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Article ; Online: Frontiers in fatty liver: recent advances in pathogenic mechanisms, assessment of patients' prognosis and pharmacotherapy : MASLD: new pathogenic mechanisms, risk assessment tools and drug therapies.

Fernández-Barrena, Maite G / Avila, Matías A

2023 Volume 79, Issue 4, Page(s) 811–813

MeSH term(s)	Humans ; Fatty Liver ; Prognosis ; Risk Assessment
Language	English
Publishing date	2023-10-21
Publishing country	Spain
Document type	Editorial
ZDB-ID	1325104-1
ISSN	1877-8755 ; 0034-9402 ; 1138-7548
ISSN (online)	1877-8755
ISSN	0034-9402 ; 1138-7548
DOI	10.1007/s13105-023-00992-y
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Article ; Online: Hepatic progenitor cells, senescence and IL-6 as the main players in combined hepatocellular-cholangiocarcinoma development.

Arechederra, María / Fernández-Barrena, Maite G

Journal of hepatology

2022 Volume 77, Issue 6, Page(s) 1479–1481

MeSH term(s)	Humans ; Carcinoma, Hepatocellular/pathology ; Interleukin-6 ; Liver Neoplasms/pathology ; Cholangiocarcinoma/pathology ; Bile Duct Neoplasms/pathology ; Bile Ducts, Intrahepatic/pathology ; Stem Cells
Chemical Substances	Interleukin-6
Language	English
Publishing date	2022-09-21
Publishing country	Netherlands
Document type	Editorial ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2022.09.008
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Zs.A 2027: Show issues

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Article ; Online: Loss of liver function in chronic liver disease: An identity crisis.

Berasain, Carmen / Arechederra, Maria / Argemí, Josepmaria / Fernández-Barrena, Maite G / Avila, Matías A

Journal of hepatology

2022 Volume 78, Issue 2, Page(s) 401–414

Abstract: Adult hepatocyte identity is constructed throughout embryonic development and fine-tuned after birth. A multinodular network of transcription factors, along with pre-mRNA splicing regulators, define the transcriptome, which encodes the proteins needed to ...

Abstract	Adult hepatocyte identity is constructed throughout embryonic development and fine-tuned after birth. A multinodular network of transcription factors, along with pre-mRNA splicing regulators, define the transcriptome, which encodes the proteins needed to perform the complex metabolic and secretory functions of the mature liver. Transient hepatocellular dedifferentiation can occur as part of the regenerative mechanisms triggered in response to acute liver injury. However, persistent downregulation of key identity genes is now accepted as a strong determinant of organ dysfunction in chronic liver disease, a major global health burden. Therefore, the identification of core transcription factors and splicing regulators that preserve hepatocellular phenotype, and a thorough understanding of how these networks become disrupted in diseased hepatocytes, is of high clinical relevance. In this context, we review the key players in liver differentiation and discuss in detail critical factors, such as HNF4α, whose impairment mediates the breakdown of liver function. Moreover, we present compelling experimental evidence demonstrating that restoration of core transcription factor expression in a chronically injured liver can reset hepatocellular identity, improve function and ameliorate structural abnormalities. The possibility of correcting the phenotype of severely damaged and malfunctional livers may reveal new therapeutic opportunities for individuals with cirrhosis and advanced liver disease.
MeSH term(s)	Humans ; Identity Crisis ; Liver Diseases/metabolism ; Liver/metabolism ; Hepatocytes/metabolism ; Transcription Factors/metabolism ; Hepatocyte Nuclear Factor 4/genetics ; Hepatocyte Nuclear Factor 4/metabolism
Chemical Substances	Transcription Factors ; Hepatocyte Nuclear Factor 4
Language	English
Publishing date	2022-09-15
Publishing country	Netherlands
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2022.09.001
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Article ; Online: SLU7: A New Hub of Gene Expression Regulation-From Epigenetics to Protein Stability in Health and Disease.

Gárate-Rascón, María / Recalde, Miriam / Rojo, Carla / Fernández-Barrena, Maite G / Ávila, Matías A / Arechederra, María / Berasain, Carmen

International journal of molecular sciences

2022 Volume 23, Issue 21

Abstract: SLU7 (Splicing factor synergistic lethal with U5 snRNA 7) was first identified as a splicing factor necessary for the correct selection of 3' splice sites, strongly impacting on the diversity of gene transcripts in a cell. More recent studies have ... ...

Abstract	SLU7 (Splicing factor synergistic lethal with U5 snRNA 7) was first identified as a splicing factor necessary for the correct selection of 3' splice sites, strongly impacting on the diversity of gene transcripts in a cell. More recent studies have uncovered new and non-redundant roles of SLU7 as an integrative hub of different levels of gene expression regulation, including epigenetic DNA remodeling, modulation of transcription and protein stability. Here we review those findings, the multiple factors and mechanisms implicated as well as the cellular functions affected. For instance, SLU7 is essential to secure liver differentiation, genome integrity acting at different levels and a correct cell cycle progression. Accordingly, the aberrant expression of SLU7 could be associated with human diseases including cancer, although strikingly, it is an essential survival factor for cancer cells. Finally, we discuss the implications of SLU7 in pathophysiology, with particular emphasis on the progression of liver disease and its possible role as a therapeutic target in human cancer.
MeSH term(s)	Humans ; Ribonucleoproteins, Small Nuclear/genetics ; RNA Splicing ; RNA Splicing Factors/genetics ; RNA Splice Sites ; Epigenesis, Genetic ; Protein Stability ; Alternative Splicing
Chemical Substances	Ribonucleoproteins, Small Nuclear ; RNA Splicing Factors ; RNA Splice Sites ; SLU7 protein, human
Language	English
Publishing date	2022-11-02
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms232113411
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Article ; Online: Epigenetic Mechanisms in Hepatic Stellate Cell Activation During Liver Fibrosis and Carcinogenesis.

Barcena-Varela, Marina / Colyn, Leticia / Fernandez-Barrena, Maite G

International journal of molecular sciences

2019 Volume 20, Issue 10

Abstract: Liver fibrosis is an essential component of chronic liver disease (CLD) and hepatocarcinogenesis. The fibrotic stroma is a consequence of sustained liver damage combined with exacerbated extracellular matrix (ECM) accumulation. In this context, ... ...

Abstract	Liver fibrosis is an essential component of chronic liver disease (CLD) and hepatocarcinogenesis. The fibrotic stroma is a consequence of sustained liver damage combined with exacerbated extracellular matrix (ECM) accumulation. In this context, activation of hepatic stellate cells (HSCs) plays a key role in both initiation and perpetuation of fibrogenesis. These cells suffer profound remodeling of gene expression in this process. This review is focused on the epigenetic alterations participating in the transdifferentiation of HSCs from the quiescent to activated state. Recent advances in the field of DNA methylation and post-translational modifications (PTM) of histones (acetylation and methylation) patterns are discussed here, together with altered expression and activity of epigenetic remodelers. We also consider recent advances in translational approaches, including the use of epigenetic marks as biomarkers and the promising antifibrotic properties of epigenetic drugs that are currently being used in patients.
MeSH term(s)	Animals ; Carcinogenesis/genetics ; DNA Methylation ; Epigenesis, Genetic ; Hepatic Stellate Cells ; Humans ; Liver ; Liver Cirrhosis/genetics
Language	English
Publishing date	2019-05-21
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms20102507
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Article ; Online: Chromatin dynamics during liver regeneration.

Arechederra, Maria / Berasain, Carmen / Avila, Matias A / Fernández-Barrena, Maite G

Seminars in cell & developmental biology

2019 Volume 97, Page(s) 38–46

Abstract: Liver regeneration is the most important reaction of the liver to an injury. Indeed, the liver possesses an extraordinary regenerative capacity orchestrated by a highly coordinated response of all the different cell types in order to recover the tissue ... ...

Abstract	Liver regeneration is the most important reaction of the liver to an injury. Indeed, the liver possesses an extraordinary regenerative capacity orchestrated by a highly coordinated response of all the different cell types in order to recover the tissue lost, while maintaining homeostasis and all the hepatic functions. To achieve this impressive physiological accomplishment, the liver experiences a transient but precisely controlled transcriptional reprogramming that allows the simultaneous activation and silencing of multiple genes at different stages of the regeneration process. Epigenetic events play a fundamental role in the organization of chromatin architecture and hence in the tight control of gene transcription. In this review, we will summarize the most relevant epigenetic modifications associated with the critical changes in gene expression and cellular behavior occurring during liver regeneration. We will discuss the relevance of DNA methylation, histone modifications, and chromatin remodelers, and the interplay between these epigenetic events, during the regeneration process, mainly after partial hepatectomy or after chemical injury.
MeSH term(s)	Chromatin/metabolism ; Epigenesis, Genetic/genetics ; Humans ; Liver Regeneration/drug effects
Chemical Substances	Chromatin
Language	English
Publishing date	2019-04-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1312473-0
ISSN	1096-3634 ; 1084-9521
ISSN (online)	1096-3634
ISSN	1084-9521
DOI	10.1016/j.semcdb.2019.03.004
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Zs.A 2918: Show issues

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Article ; Online: Epigenetics in hepatocellular carcinoma development and therapy: The tip of the iceberg.

Fernández-Barrena, Maite G / Arechederra, María / Colyn, Leticia / Berasain, Carmen / Avila, Matias A

JHEP reports : innovation in hepatology

2020 Volume 2, Issue 6, Page(s) 100167

Abstract: Hepatocellular carcinoma (HCC) is a deadly tumour whose causative agents are generally well known, but whose pathogenesis remains poorly understood. Nevertheless, key genetic alterations are emerging from a heterogeneous molecular landscape, providing ... ...

Abstract	Hepatocellular carcinoma (HCC) is a deadly tumour whose causative agents are generally well known, but whose pathogenesis remains poorly understood. Nevertheless, key genetic alterations are emerging from a heterogeneous molecular landscape, providing information on the tumorigenic process from initiation to progression. Among these molecular alterations, those that affect epigenetic processes are increasingly recognised as contributing to carcinogenesis from preneoplastic stages. The epigenetic machinery regulates gene expression through intertwined and partially characterised circuits involving chromatin remodelers, covalent DNA and histone modifications, and dedicated proteins reading these modifications. In this review, we summarise recent findings on HCC epigenetics, focusing mainly on changes in DNA and histone modifications and their carcinogenic implications. We also discuss the potential drugs that target epigenetic mechanisms for HCC treatment, either alone or in combination with current therapies, including immunotherapies.
Language	English
Publishing date	2020-08-07
Publishing country	Netherlands
Document type	Journal Article ; Review
ISSN	2589-5559
ISSN (online)	2589-5559
DOI	10.1016/j.jhepr.2020.100167
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Article: Epigenetic Biomarkers for the Diagnosis and Treatment of Liver Disease.

Arechederra, María / Recalde, Miriam / Gárate-Rascón, María / Fernández-Barrena, Maite G / Ávila, Matías A / Berasain, Carmen

Cancers

2021 Volume 13, Issue 6

Abstract: Research in the last decades has demonstrated the relevance of epigenetics in controlling gene expression to maintain cell homeostasis, and the important role played by epigenome alterations in disease development. Moreover, the reversibility of ... ...

Abstract	Research in the last decades has demonstrated the relevance of epigenetics in controlling gene expression to maintain cell homeostasis, and the important role played by epigenome alterations in disease development. Moreover, the reversibility of epigenetic marks can be harnessed as a therapeutic strategy, and epigenetic marks can be used as diagnosis biomarkers. Epigenetic alterations in DNA methylation, histone post-translational modifications (PTMs), and non-coding RNA (ncRNA) expression have been associated with the process of hepatocarcinogenesis. Here, we summarize epigenetic alterations involved in the pathogenesis of chronic liver disease (CLD), particularly focusing on DNA methylation. We also discuss their utility as epigenetic biomarkers in liquid biopsy for the diagnosis and prognosis of hepatocellular carcinoma (HCC). Finally, we discuss the potential of epigenetic therapeutic strategies for HCC treatment.
Language	English
Publishing date	2021-03-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13061265
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Article ; Online: New molecular interactions of c-Myc in cholangiocarcinoma may open new therapeutic opportunities.

Berasain, Carmen / Fernández-Barrena, Maite G / Avila, Matías A

Hepatology (Baltimore, Md.)

2016 Volume 64, Issue 2, Page(s) 336–339

Language	English
Publishing date	2016-08
Publishing country	United States
Document type	Editorial
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1002/hep.28607
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Zs.A 1660: Show issues

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Article ; Online: New insights into the regulation of bile acids synthesis during the early stages of liver regeneration: A human and experimental study.

Uriarte, Iker / Santamaria, Eva / López-Pascual, Amaya / Monte, María J / Argemí, Josepmaria / Latasa, M Ujue / Adán-Villaescusa, Elena / Irigaray, Ainara / Herranz, Jose M / Arechederra, María / Basualdo, Jorge / Lucena, Felipe / Corrales, Fernando J / Rotellar, Fernando / Pardo, Fernando / Merlen, Gregory / Rainteau, Dominique / Sangro, Bruno / Tordjmann, Thierry /

Berasain, Carmen / Marín, Jose J G / Fernández-Barrena, Maite G / Herrero, Ignacio / Avila, Matias A

Biochimica et biophysica acta. Molecular basis of disease

2024 Volume 1870, Issue 5, Page(s) 167166

Abstract: Background and aims: Liver regeneration is essential for the preservation of homeostasis and survival. Bile acids (BAs)-mediated signaling is necessary for liver regeneration, but BAs levels need to be carefully controlled to avoid hepatotoxicity. We ... ...

Abstract	Background and aims: Liver regeneration is essential for the preservation of homeostasis and survival. Bile acids (BAs)-mediated signaling is necessary for liver regeneration, but BAs levels need to be carefully controlled to avoid hepatotoxicity. We studied the early response of the BAs-fibroblast growth factor 19 (FGF19) axis in healthy individuals undergoing hepatectomy for living donor liver transplant. We also evaluated BAs synthesis in mice upon partial hepatectomy (PH) and acute inflammation, focusing on the regulation of cytochrome-7A1 (CYP7A1), a key enzyme in BAs synthesis from cholesterol. Methods: Serum was obtained from twelve human liver donors. Mice underwent 2/3-PH or sham-operation. Acute inflammation was induced with bacterial lipopolysaccharide (LPS) in mice fed control or antoxidant-supplemented diets. BAs and 7α-hydroxy-4-cholesten-3-one (C4) levels were measured by HPLC-MS/MS; serum FGF19 by ELISA. Gene expression and protein levels were analyzed by RT-qPCR and western-blot. Results: Serum BAs levels increased after PH. In patients with more pronounced hypercholanemia, FGF19 concentrations transiently rose, while C4 levels (a readout of CYP7A1 activity) dropped 2 h post-resection in all cases. Serum BAs and C4 followed the same pattern in mice 1 h after PH, but C4 levels also dropped in sham-operated and LPS-treated animals, without marked changes in CYP7A1 protein levels. LPS-induced serum C4 decline was attenuated in mice fed an antioxidant-supplemented diet. Conclusions: In human liver regeneration FGF19 upregulation may constitute a protective response from BAs excess during liver regeneration. Our findings suggest the existence of post-translational mechanisms regulating CYP7A1 activity, and therefore BAs synthesis, independent from CYP7A1/Cyp7a1 gene transcription.
Language	English
Publishing date	2024-04-19
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2024.167166
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