scispace - formally typeset
Journal ArticleDOI

Hepatic microcirculation and mechanisms of portal hypertension.

TLDR
The present Review describes the current knowledge of liver microcirculatory dysfunction in cirrhotic portal hypertension and appraise the preclinical models used to study the liver circulation and provides a comprehensive summary of the promising therapeutic options to target the liver microvasculature in Cirrhosis.
Abstract
The liver microcirculatory milieu, mainly composed of liver sinusoidal endothelial cells (LSECs), hepatic stellate cells (HSCs) and hepatic macrophages, has an essential role in liver homeostasis, including in preserving hepatocyte function, regulating the vascular tone and controlling inflammation. Liver microcirculatory dysfunction is one of the key mechanisms that promotes the progression of chronic liver disease (also termed cirrhosis) and the development of its major clinical complication, portal hypertension. In the present Review, we describe the current knowledge of liver microcirculatory dysfunction in cirrhotic portal hypertension and appraise the preclinical models used to study the liver circulation. We also provide a comprehensive summary of the promising therapeutic options to target the liver microvasculature in cirrhosis.

read more

Citations
More filters
Journal ArticleDOI

Role of liver sinusoidal endothelial cells in non-alcoholic fatty liver disease

TL;DR: Improving LSEC health appears to be a promising approach to prevent NAFLD progression and complications.
Journal ArticleDOI

Role of liver sinusoidal endothelial cells in liver diseases.

TL;DR: In this article, the main functions and phenotypic dysregulations of sinusoidal endothelial cells (LSECs) in liver diseases, specifically in the context of acute injury (ischaemia-reperfusion injury, drug-induced liver injury and bacterial and viral infection), chronic liver disease (metabolism-associated liver disease, alcoholic steatohepatitis and chronic hepatotoxic injury) and hepatocellular carcinoma, and provides a comprehensive update of the role of LSECs as therapeutic targets for liver disease.
Journal ArticleDOI

Pathophysiology of decompensated cirrhosis: Portal hypertension, circulatory dysfunction, inflammation, metabolism and mitochondrial dysfunction.

TL;DR: In this article, a review amalgamates the latest knowledge on disease mechanisms that lead to tissue injury and extrahepatic organ failure - such as systemic inflammation, mitochondrial dysfunction, oxidative stress and metabolic changes - and marries these with the classical paradigms of acute decompensation to form a single paradigm.
Journal ArticleDOI

Pan-PPAR agonist lanifibranor improves portal hypertension and hepatic fibrosis in experimental advanced chronic liver disease.

TL;DR: This study demonstrates that lanifibranor exerts clear beneficial effects in pre-clinical models of decompensated cirrhosis, which lead to amelioration in fibrosis and portal hypertension.
References
More filters
Journal ArticleDOI

Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors.

TL;DR: Induction of pluripotent stem cells from mouse embryonic or adult fibroblasts by introducing four factors, Oct3/4, Sox2, c-Myc, and Klf4, under ES cell culture conditions is demonstrated and iPS cells, designated iPS, exhibit the morphology and growth properties of ES cells and express ES cell marker genes.
Journal ArticleDOI

Global burden of NAFLD and NASH: trends, predictions, risk factors and prevention

TL;DR: The large number of patients with NAFLD with potential for progressive liver disease creates challenges for screening, as the diagnosis of NASH necessitates invasive liver biopsy.
Journal ArticleDOI

Reprint of: Extracellular matrix as a biological scaffold material: Structure and function.

TL;DR: An overview of the composition and structure of selected ECM scaffolding materials, the effects of manufacturing methods upon the structural properties and resulting mechanical behavior of the scaffold materials, and the in vivo degradation and remodeling of ECm scaffolds with an emphasis on tissue function is provided.
Related Papers (5)