scispace - formally typeset
Open AccessJournal ArticleDOI

Mechanisms of hepatic fibrogenesis

Reads0
Chats0
TLDR
Uncovering the intricate mechanisms that underlie liver fibrogenesis forms the basis for efforts to develop targeted therapies to reverse the fibrotic response and improve the outcomes of patients with chronic liver disease.
Abstract
Multiple etiologies of liver disease lead to liver fibrosis through integrated signaling networks that regulate the deposition of extracellular matrix. This cascade of responses drives the activation of hepatic stellate cells (HSCs) into a myofibroblast-like phenotype that is contractile, proliferative and fibrogenic. Collagen and other extracellular matrix (ECM) components are deposited as the liver generates a wound-healing response to encapsulate injury. Sustained fibrogenesis leads to cirrhosis, characterized by a distortion of the liver parenchyma and vascular architecture. Uncovering the intricate mechanisms that underlie liver fibrogenesis forms the basis for efforts to develop targeted therapies to reverse the fibrotic response and improve the outcomes of patients with chronic liver disease.

read more

Citations
More filters
Journal ArticleDOI

Hepatic stellate cells in liver development, regeneration, and cancer

TL;DR: Recent advances in understanding of the formation and characteristics of hepatic stellate cells, as well as their function in liver development, regeneration, and cancer are summarized and evaluated.
Journal ArticleDOI

TGF-β/SMAD Pathway and Its Regulation in Hepatic Fibrosis.

TL;DR: The role and molecular mechanisms of TGF-β/SMAD in the pathogenesis of hepatic fibrosis are discussed, and the possibility of novel therapeutic approaches to liver fibrotic disease is addressed by targeting to TGF -β/ SMAD signaling.
Journal ArticleDOI

Liver Fibrosis: Mechanistic Concepts and Therapeutic Perspectives

TL;DR: In this paper, the authors summarized cellular drivers and molecular mechanisms of fibrogenesis in chronic liver diseases and discuss their impact for the development of urgently needed anti-fibrotic therapies.
Journal ArticleDOI

IL-1β Production through the NLRP3 Inflammasome by Hepatic Macrophages Links Hepatitis C Virus Infection with Liver Inflammation and Disease

TL;DR: RNA sequencing analysis comparing THP1 cells and chronic hepatitis C patient liver demonstrates that viral engagement of the NLRP3 inflammasome stimulates IL-1β production to drive proinflammatory cytokine, chemokine, and immune-regulatory gene expression networks linked with HCV disease severity.
References
More filters
Journal ArticleDOI

Hepatic Stellate Cells: Protean, Multifunctional, and Enigmatic Cells of the Liver

TL;DR: The hepatic stellate cell has surprised and engaged physiologists, pathologists, and hepatologists for over 130 years, yet clear evidence of its role in hepatic injury and fibrosis only emerged following the refinement of methods for its isolation and characterization.
Journal ArticleDOI

TLR4 enhances TGF-beta signaling and hepatic fibrosis.

TL;DR: Modulation of TGF-β signaling by a TLR4-MyD88–NF-κB axis provides a novel link between proinflammatory and profibrogenic signals.
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

Targeting microRNAs in cancer: rationale, strategies and challenges.

TL;DR: The role of miRNAAs in tumorigenesis is described and the rationale, the strategies and the challenges for the therapeutic targeting of miRNAs in cancer are critically discussed.
Journal ArticleDOI

Macrophages: master regulators of inflammation and fibrosis.

TL;DR: Although collagen-secreting myofibroblasts once were thought of as the master "producers" of fibrosis, this review will illustrate how macrophages function as the Master "regulators" of Fibrosis.
Related Papers (5)