Gut-derived low-grade endotoxaemia, atherothrombosis and cardiovascular disease DOI Open Access
Francesco Violi, Vittoria Cammisotto,

Simona Bartimoccia

и другие.

Nature Reviews Cardiology, Год журнала: 2022, Номер 20(1), С. 24 - 37

Опубликована: Июль 15, 2022

Язык: Английский

Hepatocellular carcinoma DOI Open Access
Josep M. Llovet, Robin Kate Kelley, Augusto Villanueva

и другие.

Nature Reviews Disease Primers, Год журнала: 2021, Номер 7(1)

Опубликована: Янв. 21, 2021

Язык: Английский

Процитировано

4449

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

1254

Immunotherapies for hepatocellular carcinoma DOI
Josep M. Llovet, Florian Castet, Mathias Heikenwälder

и другие.

Nature Reviews Clinical Oncology, Год журнала: 2021, Номер 19(3), С. 151 - 172

Опубликована: Ноя. 11, 2021

Язык: Английский

Процитировано

1164

NASH limits anti-tumour surveillance in immunotherapy-treated HCC DOI Creative Commons
Dominik Pfister, Nicolás Gonzalo Núñez, Roser Pinyol

и другие.

Nature, Год журнала: 2021, Номер 592(7854), С. 450 - 456

Опубликована: Март 24, 2021

Abstract Hepatocellular carcinoma (HCC) can have viral or non-viral causes 1–5 . Non-alcoholic steatohepatitis (NASH) is an important driver of HCC. Immunotherapy has been approved for treating HCC, but biomarker-based stratification patients optimal response to therapy unmet need 6,7 Here we report the progressive accumulation exhausted, unconventionally activated CD8 + PD1 T cells in NASH-affected livers. In preclinical models NASH-induced therapeutic immunotherapy targeted at programmed death-1 (PD1) expanded within tumours did not lead tumour regression, which indicates that immune surveillance was impaired. When given prophylactically, anti-PD1 treatment led increase incidence NASH–HCC and number size nodules, correlated with increased hepatic CXCR6 , TOX TNF cells. The HCC triggered by prevented depletion neutralization, suggesting help induce NASH–HCC, rather than invigorating executing surveillance. We found similar phenotypic functional profiles from humans NAFLD NASH. A meta-analysis three randomized phase III clinical trials tested inhibitors PDL1 (programmed death-ligand 1) more 1,600 advanced revealed improve survival two additional cohorts, NASH-driven who received anti-PDL1 showed reduced overall compared other aetiologies. Collectively, these data show particularly might be less responsive immunotherapy, probably owing NASH-related aberrant cell activation causing tissue damage leads impaired Our provide a rationale according underlying aetiology studies as primary adjuvant treatment.

Язык: Английский

Процитировано

938

Liver Fibrosis: Mechanistic Concepts and Therapeutic Perspectives DOI Creative Commons

Natascha Roehlen,

Émilie Crouchet,

Thomas F. Baumert

и другие.

Cells, Год журнала: 2020, Номер 9(4), С. 875 - 875

Опубликована: Апрель 3, 2020

Liver fibrosis due to viral or metabolic chronic liver diseases is a major challenge of global health. Correlating with disease progression, key factor for outcome and risk hepatocellular carcinoma (HCC). Despite different mechanism primary injury disease-specific cell responses, the progression fibrotic follows shared patterns across main etiologies. Scientific discoveries within last decade have transformed understanding mechanisms fibrosis. Removal elimination causative agent such as control cure infection has shown that reversible. However, reversal often occurs too slowly infrequent avoid life-threatening complications particularly in advanced Thus, there huge unmet medical need anti-fibrotic therapies prevent HCC development. while many candidate agents robust effects experimental animal models, their clinical trials been limited absent. no approved therapy exists In this review we summarize cellular drivers molecular fibrogenesis discuss impact development urgently needed therapies.

Язык: Английский

Процитировано

851

Mechanisms of Fibrosis Development in Nonalcoholic Steatohepatitis DOI
Robert F. Schwabe, Ira Tabas, Utpal B. Pajvani

и другие.

Gastroenterology, Год журнала: 2020, Номер 158(7), С. 1913 - 1928

Опубликована: Фев. 8, 2020

Язык: Английский

Процитировано

490

Hepatic macrophages in liver homeostasis and diseases-diversity, plasticity and therapeutic opportunities DOI Open Access
Yankai Wen, Joeri Lambrecht,

Cynthia Ju

и другие.

Cellular and Molecular Immunology, Год журнала: 2020, Номер 18(1), С. 45 - 56

Опубликована: Окт. 12, 2020

Язык: Английский

Процитировано

480

The immunological and metabolic landscape in primary and metastatic liver cancer DOI
Xin Li, Pierluigi Ramadori, Dominik Pfister

и другие.

Nature reviews. Cancer, Год журнала: 2021, Номер 21(9), С. 541 - 557

Опубликована: Июль 29, 2021

Язык: Английский

Процитировано

396

Immune cell-mediated features of non-alcoholic steatohepatitis DOI Creative Commons
Thierry Huby, Emmanuel L. Gautier

Nature reviews. Immunology, Год журнала: 2021, Номер 22(7), С. 429 - 443

Опубликована: Ноя. 5, 2021

Non-alcoholic fatty liver disease (NAFLD) includes a range of hepatic manifestations, starting with steatosis and potentially evolving towards non-alcoholic steatohepatitis (NASH), cirrhosis or even hepatocellular carcinoma. NAFLD is major health burden, its incidence increasing worldwide. Although it primarily disturbed metabolism, involves several immune cell-mediated inflammatory processes, particularly when reaching the stage NASH, at which point inflammation becomes integral to progression disease. The cell landscape diverse steady state further evolves during NASH direct consequences for severity. In this Review, we discuss current concepts related role cells in onset NASH. A better understanding mechanisms by contribute pathogenesis should aid design innovative drugs target therapeutic options are limited. (NASH) serious chronic disorder prevalence Metabolic nature, also mobilizes system. Here, Huby Gautier knowledge regarding how subsets affect progression.

Язык: Английский

Процитировано

382

NAFLD as a driver of chronic kidney disease DOI Open Access
Christopher D. Byrne, Giovanni Targher

Journal of Hepatology, Год журнала: 2020, Номер 72(4), С. 785 - 801

Опубликована: Фев. 12, 2020

Язык: Английский

Процитировано

348