scispace - formally typeset
Open AccessJournal ArticleDOI

Reversibility of Liver Fibrosis and Inactivation of Fibrogenic Myofibroblasts

TLDR
Understanding the mechanism of inactivation of hepatic stellate cells on cessation of fibrogenic stimuli may identify new approaches to cause already existing activated liver fibrosis cells/myofibroblasts to revert to a quiescent-like state.
Abstract
Many studies have demonstrated that hepatic fibrosis is reversible. Regression of liver fibrosis is associated with resorption of fibrous scar and the disappearance of collagen-producing myofibroblasts. The fate of these myofibroblasts has been recently revealed: some myofibroblasts undergo senescence and apoptosis during reversal of fibrosis, whereas other myofibroblasts revert to a quiescent-like phenotype. Inactivation of myofibroblasts is a newly described phenomenon (Kisseleva et al. in Proc. Natl .Acad. Sci. USA 109:9448–9453, 2012) which now requires mechanistic investigation. Understanding the mechanism of inactivation of hepatic stellate cells on cessation of fibrogenic stimuli may identify new approaches to cause already existing activated hepatic stellate cells/myofibroblasts to revert to a quiescent-like state. This review summarizes the research on the inactivation of hepatic myofibroblasts.

read more

Content maybe subject to copyright    Report

Citations
More filters
Journal ArticleDOI

2016 Comprehensive Update of the Banff Working Group on Liver Allograft Pathology: Introduction of Antibody-Mediated Rejection.

Anthony J. Demetris, +76 more
TL;DR: New recommendations for complement component 4d tissue staining and interpretation, staging liver allograft fibrosis, and findings related to immunosuppression minimization are included.
Journal ArticleDOI

Transforming Growth Factor-β-Induced Cell Plasticity in Liver Fibrosis and Hepatocarcinogenesis.

TL;DR: Light is shed about the pleiotropic actions of TGF-β that explain its effects on the different liver cell populations, and the cross-talk with other signaling pathways that contribute to T GF-β effects, in particular the Epidermal Growth Factor Receptor (EGFR), are presented.
Journal ArticleDOI

Reversibility of liver fibrosis.

TL;DR: While most of the research has been focused on HSCs/myofibroblasts and inflammatory pathways, the crosstalk between different organs, various cell types and multiple signaling pathways should not be overlooked.
Journal ArticleDOI

New Developments on the Treatment of Liver Fibrosis

TL;DR: The current knowledge of targeting the steps in HSC activation as therapeutic target for liver fibrosis is described.
Journal ArticleDOI

Mechanisms of Lung Fibrosis Resolution

TL;DR: This review describes the current understanding of the mechanisms whereby the lung is known to resolve fibrosis focusing on degradation of the extracellular matrix, removal of myofibroblasts, and the role of inflammatory cells.
References
More filters
Journal ArticleDOI

Epithelial-mesenchymal transition and its implications for fibrosis.

TL;DR: This review highlights recent advances in the process of EMT signaling in health and disease and how it may be attenuated or reversed by selective cytokines and growth factors.
Journal ArticleDOI

Senescence of activated stellate cells limits liver fibrosis

TL;DR: In this paper, the authors show that senescent cells accumulate in murine livers treated to produce fibrosis, a precursor pathology to cirrhosis, derived primarily from activated hepatic stellate cells, which initially proliferate in response to liver damage and produce the extracellular matrix.
Journal ArticleDOI

Homozygous disruption of the murine MDR2 P-glycoprotein gene leads to a complete absence of phospholipid from bile and to liver disease

TL;DR: It is concluded that the mdr2 P-glycoprotein has an essential role in the secretion of phosphatidylcholine into bile and hypothesize that it may be a phospholipid transport protein or phospholIPid flippase.
Journal Article

Senescence of Activated Stellate Cells Limits Liver Fibrosis

TL;DR: It is shown that senescent cells accumulate in murine livers treated to produce fibrosis, a precursor pathology to cirrhosis, and natural killer cells preferentially kill senescent activated stellate cells in vitro and in vivo, thereby facilitating the resolution of fibrosis.
Related Papers (5)