Molecular and cellular mechanisms of liver fibrosis and its regression
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Summary
This Review summarizes studies of the molecular mechanisms underlying the reversibility of liver fibrosis, including apoptosis and the inactivation of hepatic stellate cells, the crosstalk between the liver and the systems that orchestrate the recruitment of bone marrow-derived macrophages driving fibrosis resolution, and the interactions between various cell types that lead to the intracellular signalling that induces fibrosis or its regression.
- Type
- review
- Published
- 2020-10-30
- Cited by
- 1,816
- References
- 299
- OpenAlex
- https://openalex.org/W3095484986
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:226205499
Keywords
Myofibroblast, Hepatic stellate cell, Fibrosis, Medicine, Extracellular matrix
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Cited by
- Mori fructus aqueous extracts attenuates liver injury by inhibiting ferroptosis via the Nrf2 pathway
- Extracellular histones stimulate collagen expression in vitro and promote liver fibrogenesis in a mouse model via the TLR4-MyD88 signaling pathway
- HBV induces liver fibrosis via the TGF-β1/miR-21-5p pathway
- The protective effects of granulocyte-macrophage colony-stimulating factor against radiation-induced lung injury
- Previous liver regeneration induces fibro-protective mechanisms during thioacetamide-induced chronic liver injury.
- Regression of portal hypertension: underlying mechanisms and therapeutic strategies
- Up‐regulation of FUT8 inhibits TGF-β1-induced activation of hepatic stellate cells during liver fibrogenesis
- A combination of pirfenidone and TGF-β inhibition mitigates cystic echinococcosis-associated hepatic injury
- Expression of Interferons Lambda 3 and 4 Induces Identical Response in Human Liver Cell Lines Depending Exclusively on Canonical Signaling
- Pathogenese und Progression der Leberzirrhose: aktuelle Perspektiven
- Experimental and Investigational Targeted Therapies for the Management of Fibrosis in NASH: An Update
- Macrophages in Chronic Liver Failure: Diversity, Plasticity and Therapeutic Targeting
- uhrf1 and dnmt1 Loss Induces an Immune Response in Zebrafish Livers Due to Viral Mimicry by Transposable Elements
- TGF‐β as a driver of fibrosis: physiological roles and therapeutic opportunities
- Infusion of Kupffer Cells Expanded in Vitro Ameliorated Liver Fibrosis in a Murine Model of Liver Injury
- Therapeutic targeting of STAT3 employing small interference RNAs and antisense oligonucleotides embedded exosomes in liver fibrosis
- Chronic Alcohol Exposure of Cells Using Controlled Alcohol-Releasing Capillaries
- Transcriptomics Identify Thrombospondin‐2 as a Biomarker for NASH and Advanced Liver Fibrosis
- Antisense Tissue Factor Oligodeoxynucleotides Protected Diethyl Nitrosamine/Carbon Tetrachloride-Induced Liver Fibrosis Through Toll Like Receptor4-Tissue Factor-Protease Activated Receptor1 Pathway
- Salidroside Inhibits CCl4-Induced Liver Fibrosis in Mice by Reducing Activation and Migration of HSC Induced by Liver Sinusoidal Endothelial Cell-Derived Exosomal SphK1
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