Biliary Atresia: Clinical and Research Challenges for the Twenty‐First Century DOI Open Access
Jorge A. Bezerra, Rebecca G. Wells, Cara L. Mack

и другие.

Hepatology, Год журнала: 2018, Номер 68(3), С. 1163 - 1173

Опубликована: Март 31, 2018

Biliary atresia (BA) is a fibroinflammatory disease of the intrahepatic and extrahepatic biliary tree. Surgical hepatic portoenterostomy (HPE) may restore bile drainage, but progression results in complications portal hypertension advanced cirrhosis most children. Recognizing that further progress field unlikely without better understanding underlying cause(s) pathogenesis disease, National Institutes Diabetes Digestive Kidney Diseases (NIDDK) sponsored research workshop focused on innovative promising approaches identifying future areas research. Investigators discussed recent advances using gestational ultrasound newborn BA screening with serum direct (conjugated) bilirubin support prenatal onset injury. Experimental human studies implicate toxic properties environmental toxins (e.g., biliatresone) viruses cytomegalovirus) to system. Among host factors, sequence variants genes related development ciliopathies, notable lack cholangiocyte glycocalyx submucosal collagen bundles neonatal ducts, an innate proinflammatory bias immune system contribute increased susceptibility damage obstruction following epithelial These form foundation for agenda factor(s) cause BA, potential use population screening, mechanisms prominent fibrosis young infants, determinations clinical surrogates progression, design trials target subgroups patients initial drainage HPE. (Hepatology 2018; 00:000-000).

Язык: Английский

Mechanisms of NAFLD development and therapeutic strategies DOI
Scott L. Friedman, Brent A. Neuschwander‐Tetri, Mary E. Rinella

и другие.

Nature Medicine, Год журнала: 2018, Номер 24(7), С. 908 - 922

Опубликована: Июнь 29, 2018

Язык: Английский

Процитировано

3354

MAFLD: A Consensus-Driven Proposed Nomenclature for Metabolic Associated Fatty Liver Disease DOI
Mohammed Eslam, Arun J. Sanyal, Jacob George

и другие.

Gastroenterology, Год журнала: 2020, Номер 158(7), С. 1999 - 2014.e1

Опубликована: Фев. 8, 2020

Язык: Английский

Процитировано

2645

Mechanisms and disease consequences of nonalcoholic fatty liver disease DOI Creative Commons
Rohit Loomba, Scott L. Friedman, Gerald I. Shulman

и другие.

Cell, Год журнала: 2021, Номер 184(10), С. 2537 - 2564

Опубликована: Май 1, 2021

Язык: Английский

Процитировано

1292

Hepatic stellate cells as key target in liver fibrosis DOI Creative Commons

Takaaki Higashi,

Scott L. Friedman, Yujin Hoshida

и другие.

Advanced Drug Delivery Reviews, Год журнала: 2017, Номер 121, С. 27 - 42

Опубликована: Май 12, 2017

Язык: Английский

Процитировано

1204

The gut–liver axis and the intersection with the microbiome DOI
Anupriya Tripathi, Justine W. Debelius, David A. Brenner

и другие.

Nature Reviews Gastroenterology & Hepatology, Год журнала: 2018, Номер 15(7), С. 397 - 411

Опубликована: Май 10, 2018

Язык: Английский

Процитировано

1124

Role of oxidative stress in the pathogenesis of nonalcoholic fatty liver disease DOI Creative Commons
Ze Chen, Ruifeng Tian, Zhi‐Gang She

и другие.

Free Radical Biology and Medicine, Год журнала: 2020, Номер 152, С. 116 - 141

Опубликована: Март 8, 2020

Nonalcoholic fatty liver disease (NAFLD) has emerged as the most common chronic worldwide and is strongly associated with presence of oxidative stress. Disturbances in lipid metabolism lead to hepatic accumulation, which affects different reactive oxygen species (ROS) generators, including mitochondria, endoplasmic reticulum, NADPH oxidase. Mitochondrial function adapts NAFLD mainly through downregulation electron transport chain (ETC) preserved or enhanced capacity mitochondrial acid oxidation, stimulates ROS overproduction within ETC components upstream cytochrome c However, non-ETC sources ROS, particular, β-oxidation, appear produce more metabolic diseases. Endoplasmic reticulum stress oxidase alterations are also NAFLD, but degree their contribution remains unclear. Increased generation induces changes insulin sensitivity expression activity key enzymes involved metabolism. Moreover, interaction between redox signaling innate immune forms a complex network that regulates inflammatory responses. Based on mechanistic view described above, this review summarizes mechanisms may account for excessive production potential roles drive progression, therapeutic interventions related

Язык: Английский

Процитировано

952

Gut microbiota and human NAFLD: disentangling microbial signatures from metabolic disorders DOI
Judith Aron‐Wisnewsky, Chloé Vigliotti, Julia J. Witjes

и другие.

Nature Reviews Gastroenterology & Hepatology, Год журнала: 2020, Номер 17(5), С. 279 - 297

Опубликована: Март 9, 2020

Язык: Английский

Процитировано

787

Triggering and resolution of inflammation in NASH DOI

Susanne Schuster,

Daniel Cabrera, Marco Arrese

и другие.

Nature Reviews Gastroenterology & Hepatology, Год журнала: 2018, Номер 15(6), С. 349 - 364

Опубликована: Май 8, 2018

Язык: Английский

Процитировано

751

Lipotoxicity and the gut-liver axis in NASH pathogenesis DOI
Fabio Marra, Gianluca Svegliati‐Baroni

Journal of Hepatology, Год журнала: 2017, Номер 68(2), С. 280 - 295

Опубликована: Ноя. 14, 2017

Язык: Английский

Процитировано

701

Suppressed hepatic bile acid signalling despite elevated production of primary and secondary bile acids in NAFLD DOI
Na Jiao, Susan S. Baker,

Adrián Chapa‐Rodríguez

и другие.

Gut, Год журнала: 2017, Номер 67(10), С. 1881 - 1891

Опубликована: Авг. 3, 2017

Objective Bile acids are regulators of lipid and glucose metabolism, modulate inflammation in the liver other tissues. Primary bile such as cholic acid chenodeoxycholic (CDCA) produced liver, converted into secondary deoxycholic (DCA) lithocholic by gut microbiota. Here we investigated possible roles non-alcoholic fatty disease (NAFLD) pathogenesis impact microbiome on signalling NAFLD. Design Serum levels fibroblast growth factor 19 (FGF19), gene expression profiles compositions were determined patients with NAFLD, high-fat diet-fed rats their controls. Results concentrations primary increased In per cent, farnesoid X receptor (FXR) antagonistic DCA was increased, while agonistic CDCA decreased Increased mRNA for cytochrome P450 7A1, Na + -taurocholate cotransporting polypeptide paraoxonase 1, no change small heterodimer partner salt export pump, reduced serum FGF19 evidence impaired FXR 4 (FGFR4)-mediated Taurine glycine metabolising bacteria reflecting production. Similar changes observed rats. Conclusions The profile, hepatic pattern composition consistently support an elevated production proportion explains, at least part, suppression FXR-mediated FGFR4-mediated signalling. Our study suggests that future NAFLD intervention may target components signalling, including converting microbiome.

Язык: Английский

Процитировано

573