Modelling human liver disease: from steatotic liver disease to MASH-HCC DOI
Christian Stoess, Ariel E. Feldstein

Nature Reviews Endocrinology, Год журнала: 2024, Номер unknown

Опубликована: Окт. 24, 2024

Язык: Английский

A Guide to Pathophysiology, Signaling Pathways, and Preclinical Models of Liver Fibrosis DOI

Marjia Sultana,

Md Asrarul Islam,

Rhema Khairnar

и другие.

Molecular and Cellular Endocrinology, Год журнала: 2025, Номер unknown, С. 112448 - 112448

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

2

LARP6 regulates the mRNA translation of fibrogenic genes in liver fibrosis DOI Open Access
Hyun Young Kim, Orel Mizrahi,

Wonseok Lee

и другие.

bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2025, Номер unknown

Опубликована: Янв. 18, 2025

Summary Metabolic syndrome and excessive alcohol consumption result in liver injury fibrosis, which is characterized by increased collagen production activated Hepatic Stellate Cells (HSCs). LARP6, an RNA-binding protein, was shown to facilitate production. However, LARP6 expression functionality as a regulator of fibrosis development disease relevant model remains elusive. By using snRNA-sequencing, we show that upregulated mainly HSCs patients. Moreover, knockdown human suppresses fibrogenic gene expression. integrating eCLIP analysis ribosome profiling HSCs, interacts with mature mRNAs comprising over 300 genes, including RNA structural elements within COL1A1 , COL1A2 COL3A1 regulate mRNA translation. Furthermore, HSC attenuates spheroids. Altogether, our results suggest targeting may provide new strategies for anti-fibrotic therapy. Highlights HSCs. reduces development. Of the hundreds targets, most mRNAs. regulates translation via interaction 5’UTRs.

Язык: Английский

Процитировано

0

Multi-Modal Analysis of human Hepatic Stellate Cells identifies novel therapeutic targets for Metabolic Dysfunction-Associated Steatotic Liver Disease DOI Creative Commons
Hyun Young Kim, Sara Brin Rosenthal, Xiao Liu

и другие.

Journal of Hepatology, Год журнала: 2024, Номер unknown

Опубликована: Ноя. 1, 2024

Metabolic dysfunction-associated steatotic liver disease (MASLD) ranges from (MASL) to steatohepatitis (MASH) with fibrosis. Activation of Hepatic Stellate Cells (HSCs) into fibrogenic myofibroblasts plays a critical role in the pathogenesis MASH We compared transcriptome and chromatin accessibility human HSCs NORMAL, MASL, livers at single cell resolution. aimed identify genes that are upregulated activated determine which these key

Язык: Английский

Процитировано

4

d4-Cystamine: A Deuterated Cystamine Derivative with Improved Anti-Inflammatory and Anti-Fibrotic Activities in a Murine Model of Fibrosing Steatohepatitis DOI Creative Commons
Aleksandra Leszczynska, Thibault Alle, Benedikt Kaufmann

и другие.

ACS Pharmacology & Translational Science, Год журнала: 2025, Номер 8(3), С. 885 - 898

Опубликована: Фев. 24, 2025

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a multifactorial chronic that can progress to metabolic steatohepatitis (MASH) and fibrosis, ultimately leading cirrhosis hepatocellular carcinoma. Oxidative stress believed play an important role in the development of MASH. Small aminothiol compounds such as cysteamine its oxidized precursor, cystamine, are known pleiotropic exhibit relatively potent antioxidant other effects. Herein, we evaluate efficacy well two deuterated derivatives, choline-deficient, L-amino acid-defined, high-fat-diet (CDAA-HFD) mouse model rapidly progressing fibrosis. Compared control mice, daily oral administration isotopically reinforced cystamine derivatives (200 mg/kg) led significant reduction fibrosis inflammation oxidative stress. Moreover, treatment appeared increase with deuteration state tetradeuterated derivative, d 4 -cystamine, being most effective. These results indicate hold promise potential candidates for

Язык: Английский

Процитировано

0

Decoding Liver Fibrosis: How Omics Technologies and Innovative Modeling Can Guide Precision Medicine DOI Open Access

Gabriele Codotto,

Benedetta Blarasin,

Claudio Tiribelli

и другие.

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(6), С. 2658 - 2658

Опубликована: Март 15, 2025

The burden of chronic liver disease (CLD) is dramatically increasing. It estimated that 20–30% the population worldwide affected by CLD. Hepatic fibrosis a symptom common to all CLDs. Although it affects functional activities, reversible stage if diagnosed at an early stage, but no resolutive therapy contrast currently available. Therefore, efforts are needed study molecular insights disease. Emerging cutting-edge fields in cellular and biology introducing innovative strategies. Spatial single-cell resolution approaches paving way for more detailed understanding mechanisms underlying fibrosis. Cellular models have been generated recapitulate in-a-dish pathophysiology fibrosis, yielding remarkable results not only uncover also serve as patient-specific avatars precision medicine. Induced pluripotent stem cells (iPSC) organoids incredible tools reshape modeling diseases, describe their architecture, residents hepatic tissue heterogeneous population. present work aims give overview omics technologies revolutionizing research current model this

Язык: Английский

Процитировано

0

DHCR7 inhibition ameliorates MetALD and HCC in mice and human 3D liver spheroids DOI Creative Commons
Gen Yamamoto,

Raquel Carvalho‐Gontijo Weber,

Wonseok Lee

и другие.

JHEP Reports, Год журнала: 2025, Номер unknown, С. 101415 - 101415

Опубликована: Апрель 1, 2025

Язык: Английский

Процитировано

0

Towards more consistent models and consensual terminology in preclinical research for Steatotic Liver Disease DOI Creative Commons
Abraham S. Meijnikman, Marcos F. Fondevila, Marco Arrese

и другие.

Journal of Hepatology, Год журнала: 2024, Номер unknown

Опубликована: Ноя. 1, 2024

Язык: Английский

Процитировано

1

Modelling human liver disease: from steatotic liver disease to MASH-HCC DOI
Christian Stoess, Ariel E. Feldstein

Nature Reviews Endocrinology, Год журнала: 2024, Номер unknown

Опубликована: Окт. 24, 2024

Язык: Английский

Процитировано

0