Latest News On Fibrosis Archives 2012
2016 - Fibrosis/Cirrhosis/Liver Cancer/Transplants
Association Between Sustained Virological Response and All-Cause Mortality Among Patients With Chronic Hepatitis C and Advanced Hepatic Fibrosis: "In conclusion, our study indicates that SVR was associated with improved overall survival in patients with chronic HCV infection and advanced hepatic fibrosis."
GCS-100 Demonstrates Statistically Significant Reduction in Liver Fibrosis
Hepatic fibrosis, not NAFLD, increased risk for cardiovascular-related death
Monoclonal antibody GS-6624 well tolerated by patients with hepatic fibrosis in initial safety study
Galectin Receives US Patent for Second Drug Class to Treat Chronic Liver Disease with Fibrosis (Scarring) and Cirrhosis
Chronic HCV infection: epidemiological and clinical relevance
AASLD- Data from Phase 2B Trials of Simeprevir (TMC435) in Hepatitis C Patients with Advanced Fibrosis
Genomics and HCV infection: Progression of fibrosis and treatment response
Inhibition of enzyme NOX4 prevents liver fibrosis
Checkmate to liver biopsy in chronic hepatitis C?
AASLD 2012-Galectin Therapeutics to Present New Data on the Treatment of Fatty Liver Disease and Fibrosis
Protease Inhibitors - Maximizing Treatment Benefit in HCV
Reduction in hepatic inflammation associated with less fibrosis progression in HCV
Severity of Fibrosis in Women with Hepatitis C
New 'Traffic Light' Test Could Save Lives With Earlier Diagnosis Of Liver Disease
Drug Successfully Halts Fibrosis in Animal Model of Liver Disease
A Debate on Liver Fibrosis Progression in HIV/HCV-Coinfected Patients
Fibrosis - HCV suppression reduces liver damage
FDA Submission for HepaFat™ Scan and update on Liver Fibrosis Test
Hepatitis C Treatment May Improve Liver Fibrosis Even Without a Cure
HCV: Oral Interferon Found to Reverse Thrombocytopenia; Reduced Relapse Rate Seen in Patients with Mild Fibrosis
Fibrosis - HCV suppression reduces liver damage
It’s Not Easy to Diagnose Intermediate-Stage Liver Fibrosis
Biopsy has a low level of diagnostic performance for liver fibrosis stages F2 and F1. The recommendation for biopsy analysis, instead of non-invasive tests, for diagnosis of intermediate stages of fibrosis is therefore misleading, according to the June issue of Clinical Gastroenterology and Hepatology.
Full Text - Reversibility of liver fibrosis
Doctors in Europe and the US disagree over the pace of liver fibrosis in men co-infected with HIV and hepatitis C
May Genomics and proteomics in liver fibrosis and cirrhosis
ibrogenesis & Tissue Repair
2012, 5:1 doi:10.1186/1755-1536-5-1
The electronic version of this article is the complete one and can be found online at:
Liver fibrosis results from a wound-healing response to chronic injury, which leads to excessive matrix, or scar deposition. This scar tissue can restrict blood flow due to contraction of the organ, leading to progressive liver damage and cirrhosis (the end stage of fibrosis), complicated by liver failure, portal hypertension and/or hepatocellular carcinoma .
Research reveals possible strategy to reverse fibrosis in liver and other organs
An international team of scientists, led by researchers at the University of
California, San Diego School of Medicine, report that significant numbers of
myofibroblasts - cells that produce the fibrous scarring in chronic liver injury
- revert to an inactive phenotype as the liver heals. The discovery in mouse
models could ultimately help lead to new human therapies for reversing fibrosis
in the liver, and in other organs like the lungs and kidneys.
The work is published in the May 7, 2012 online Early Edition of the
Proceedings of the National Academy of Sciences.
"The take-away message is two-fold," said David A. Brenner, MD, vice
chancellor for Health Sciences, dean of the UC San Diego School of Medicine and
senior author of the paper. "First, we've shown that liver fibrosis is markedly
reversible and we now better understand how it happens. Second, we can start
looking for ways to direct active myofibroblasts to stop producing scar, and
become inactive. We can focus on developing drugs that promote cell change and
regression. It raises the bar for prospective treatment tremendously."
Liver fibrosis is the 12th leading cause of death in the United States. It is
the result of chronic liver injury caused by such agents as the hepatitis B and C viruses,
alcoholic liver disease and non-alcoholic steatohepatitis.
The condition is manifested by extensive scarring of liver tissue and the organ's progressive
inability to filter body toxins. Liver fibrosis precedes the development of liver cancer.
Often, the only treatment for end-stage liver fibrosis is an organ transplant.
Fibrosis begins when infectious agents or excessive alcohol consumption trigger activation
of hepatic stellate cells (HSCs), which normally act as quiescent storage units for nutrients
like vitamin A in the liver. Once activated, these HSCs acquire characteristics of
another cell type called myofibroblasts, which are characterized by their abundant production
of extracellular matrix proteins such as collagen. These proteins accumulate as scar tissue,
rendering the organ progressively dysfunctional.
However, if the source of the liver injury is successfully treated or eliminated, the liver can repair itself.
In part, this is due to the activated HSCs undergoing apoptosis (programmed cell death) and
being removed by other cells. But UC San Diego scientists say that, in tests using a mouse model, as
many as half of all activated HSCs persist. They do not die, but rather revert
to an inactive phenotype during fibrotic regression.
Continued on Next page >>
Galectin Therapeutics Announces Long-term Engagement of Dr.Scott Friedman to Advise on Liver Fibrosis Programs
Genotype 1-Risk of Atherosclerosis Increases in Hepatitis C Patients With Fibrosis
Industry Voices: The Fibrosis Stampede
Nitric oxide augments mesenchymal stem cell ability to repair liver fibrosis
Liver fibrosis is a major health problem worldwide and poses a serious obstacle for cell basedtherapies.
Mesenchymal stem cells (MSCs) are multipotent and important candidate cells
forfuture clinical applications however success of MSC therapy depends upon
their homing andsurvival in recipient organs.
This study was designed to improve the repair potential of MSCsby transplanting them in sodium
nitroprusside (SNP) pretreated mice with CCl4 induced liver fibrosis.
Methods: SNP 100 mM, a nitric oxide (NO) donor, was administered twice a
week for 4 weeks toCCl4-injured mice. MSCs were isolated from C57BL/6 wild type
mice and transplanted in theleft lateral lobe of the liver in experimental
After 4 weeks, animals were sacrificedand liver improvement was
analyzed. Analysis of fibrosis by qRT-PCR and sirius redstaining, homing,
bilirubin and alkaline phosphatase (ALP) serum levels between
differenttreatment groups were compared to control.
Results: Liver histology demonstrated enhanced MSCs homing in SNP-MSCs group compared toMSCs
The gene expression of fibrotic markers; alphaSMA, collagen
1alpha1, TIMP, NFkappaBand iNOS was down regulated while cytokeratin 18,
albumin and eNOS was up-regulated inSNP-MSCs group. Combine treatment
sequentially reduced fibrosis in SNP-MSCs treatedliver compared to the other
These results were also comparable withreduced serum
levels of bilirubin and ALP observed in SNP-MSCs treated group.
Conclusion: This study demonstrated that NO effectively augments MSC
ability to repair liver fibrosis induced by CCl4 in mice and therefore is a
better treatment regimen to reduce liver fibrosis.
Author: Gibran AliSadia MohsinMohsin KhanGhazanfar Ali NasirSuleiman ShamsShaheen N KhanSheikh
RiazuddinCredits/Source: Journal of Translational Medicine 2012, 10:75
Vitamin D and fibrosis progression in HCV
Decreased vitamin D levels have been described in various forms of chronic liver disease and associated with advanced fibrosis....
Higher serum testosterone increases the risk of HCV–related liver disease
Higher serum testosterone is associated with an increased the risk of hepatitis C–related liver disease in males, reports the most recent of Hepatology.
Gene expression profiling of HCV genotype 3a initial liver fibrosis and cirrhosis patients using microarray
Hepatitis C virus (HCV) causes liver fibrosis that may lead to liver cirrhosis or hepatocellular carcinoma (HCC), and may partially depend on infecting viral genotype. HCV genotype 3a is being more common in Asian population, especially Pakistan; the detail mechanism of infection still needs to be explored.
In this study, we investigated and compared the gene expression profile between initial fibrosis stage and cirrhotic 3a genotype patients.
Methods: Gene expression profiling of human liver tissues was performed containing more than 22000 known genes. Using Oparray protocol, preparation and hybridization of slides was carried out and followed by scanning with GeneTAC integrator 4.0 software.
Normalization of the data was obtained using MIDAS software and Significant Microarray Analysis (SAM) was performed to obtain differentially expressed candidate genes.
Results: Out of 22000 genes studied, 219 differentially regulated genes found with P [less than or equal to] 0.05 between both groups; 107 among those were up-regulated and 112 were down-regulated. These genes were classified into 31 categories according to their biological functions.
The main categories included: apoptosis, immune response, cell signaling, kinase activity, lipid metabolism, protein metabolism, protein modulation, metabolism, vision, cell structure, cytoskeleton, nervous system, protein metabolism, protein modulation, signal transduction, transcriptional regulation and transport activity.
Conclusion: This is the first study on gene expression profiling in patients associated with genotype 3a using microarray analysis. These findings represent a broad portrait of genomic changes in early HCV associated fibrosis and cirrhosis.
We hope that identified genes in this study will help in future to act as prognostic and diagnostic markers to differentiate fibrotic patients from cirrhotic ones.
Author: Waqar AhmadBushra IjazSajida Hassan
Credits/Source: Journal of Translational Medicine 2012, 10:41
Genomics and proteomics in liver fibrosis and cirrhosis
Genomics and proteomics have become increasingly important in biomedical science in the past decade, as they provide an opportunity for hypothesis-free experiments that can yield major insights not previously foreseen when scientific and clinical questions are based only on hypothesis-driven approaches. Use of these tools, therefore, opens new avenues for uncovering physiological and pathological pathways. Liver fibrosis is a complex disease provoked by a range of chronic injuries to the liver, among which are viral hepatitis, (non-) alcoholic steatohepatitis and autoimmune disorders. Some chronic liver patients will never develop fibrosis or cirrhosis, whereas others rapidly progress towards cirrhosis in a few years......
Serum Vitamin D Levels Are Not Predictive of the Progression of Chronic Liver Disease in Hepatitis C Patients with Advanced Fibrosis