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Open AccessJournal ArticleDOI

Hepatic macrophages but not dendritic cells contribute to liver fibrosis by promoting the survival of activated hepatic stellate cells in mice

TLDR
Promotion of NF‐κB–dependent myofibroblast survival by macrophages but not DCs provides a novel link between inflammation and fibrosis.
About
This article is published in Hepatology.The article was published on 2013-10-01 and is currently open access. It has received 450 citations till now. The article focuses on the topics: Hepatic fibrosis & Hepatic stellate cell.

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Macrophages in Tissue Repair, Regeneration, and Fibrosis

Thomas A. Wynn, +1 more
- 15 Mar 2016 - 
TL;DR: This review discusses the mechanisms that instruct macrophages to adopt pro-inflammatory, pro-wound-healing,pro-fibrotic, anti- inflammatory, anti -fib rotic, Pro-resolving, and tissue-regenerating phenotypes after injury, and highlights how some of these mechanisms and macrophage activation states could be exploited therapeutically.
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Mechanisms of hepatic stellate cell activation

TL;DR: These findings reinforce the remarkable complexity and plasticity of HSC activation, and underscore the value of clarifying its regulation in hopes of advancing the development of novel diagnostics and therapies for liver disease.
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Liver fibrosis and repair: immune regulation of wound healing in a solid organ

TL;DR: This Review focuses on recent advances in liver fibrosis research as a paradigm for wound healing in solid organs and the role of the immune system in regulating and balancing this response.
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Fate tracing reveals hepatic stellate cells as dominant contributors to liver fibrosis independent of its aetiology

TL;DR: It is demonstrated that hepatic stellate cells give rise to 82-96% of myofibroblasts in models of toxic, cholestatic and fatty liver disease, and HSCs should be considered the primary cellular target for anti-fibrotic therapies across all types of liver disease.
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Liver macrophages in tissue homeostasis and disease

TL;DR: Novel findings regarding the origin, classification and function of hepatic macrophages are highlighted, and their divergent roles in the healthy and diseased liver are discussed.
References
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Journal ArticleDOI

NF-κB Antiapoptosis: Induction of TRAF1 and TRAF2 and c-IAP1 and c-IAP2 to Suppress Caspase-8 Activation

TL;DR: Tumor necrosis factor alpha binding to the TNF receptor (TNFR) potentially initiates apoptosis and activates the transcription factor nuclear factor kappa B (NF-kappaB), which suppresses apoptosis by an unknown mechanism.
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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.
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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.
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Selective depletion of macrophages reveals distinct, opposing roles during liver injury and repair

TL;DR: These data provide the first clear evidence that functionally distinct subpopulations of macrophages exist in the same tissue and that these macrophage play critical roles in both the injury and recovery phases of inflammatory scarring.
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