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An Advanced Murine Model for Nonalcoholic Steatohepatitis in Association with Type 2 Diabetes

An Advanced Murine Model for Nonalcoholic Steatohepatitis in Association with Type 2 Diabetes

Published on: April 26, 2019

Molecular Pathogenesis of NASH.

Alessandra Caligiuri¹, Alessandra Gentilini², Fabio Marra³

¹Dipartimento di Medicina Sperimentale e Clinica, Università degli Studi di Firenze, Firenze 50121, Italy. alessandra.caligiuri@unifi.it.

International Journal of Molecular Sciences

|September 23, 2016

Summary

Nonalcoholic steatohepatitis (NASH) is a major liver disease linked to metabolic syndrome. Understanding NASH pathogenesis and fibrosis is key to developing new treatments and identifying progression biomarkers.

Keywords:

chemokines fibrosis genetics hepatic stellate cells inflammation macrophages microbiota nuclear receptors pattern-recognition receptors

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Area of Science:

Hepatology and metabolic disease research.

Background:

Nonalcoholic steatohepatitis (NASH) is a leading cause of chronic liver disease in Western countries, strongly associated with obesity, diabetes, and metabolic syndrome.
NASH progression can lead to severe outcomes, including advanced fibrosis, cirrhosis, and hepatocellular carcinoma.

Approach:

This review synthesizes recent findings on the pathogenesis of NASH.
It examines the molecular and cellular events driving liver damage and fibrotic progression in NASH.
The review also considers signals from adipose tissue and the gastrointestinal tract influencing NASH.

Key Points:

Recent data on NASH pathogenesis and fibrogenic progression are discussed.
Potential therapeutic targets for NASH are highlighted.
Biomarkers for assessing NASH disease progression are identified.

Conclusions:

A deeper understanding of NASH mechanisms is crucial for effective treatment strategies.
Identifying therapeutic targets and progression biomarkers can improve patient outcomes.