Evidence map›Paper›PMID 33529675›Full record

ReviewGastroenterology2021

Fibrosis Regression After Eradication of Hepatitis C Virus: From Bench to Bedside.

Don C Rockey, Scott L Friedman

Open access · greenAbstract readReview
In one paragraph

Review in Gastroenterology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 3 pooled it
11.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

90 citing papers in PubMed, 3 syntheses or guidelines pooled it, 145 citations in OpenAlex.

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30 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

Don C RockeyThe Medical University of South Carolina, Charleston, South Carolina. Electronic address: rockey@musc.edu.
Scott L FriedmanDivision of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, New York.
Icahn School of Medicine at Mount Sinai · USMedical University of South Carolina · US

Funding

The role of SMAD1 and SATB2 in colon patterningP20GM130457 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI Evan R Delgado · 2020 to 2026
$18.7M
Proteomics CoreP30DK123704 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI Garth R Swanson · 2020 to 2026
$8.8M
The Role of KLF6 in Hepatic FibrosisR01DK056621 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI FRIEDMAN, SCOTT L. · 2000 to 2019
$6.2M
A Molecular Approach to the Pathogenesis of Portal HypertensionR01DK113159 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI DON C. ROCKEY · 2017 to 2026
$2.7M
NO AND THE CELLULAR PATHOGENESIS OF PORTAL HYPERTENSIONR01DK057830 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI ROCKEY, DON C. · 2000 to 2012
$2.6M
Hepatic stellate cells in NASH fibrosis and HCCR01DK128289 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI SCOTT L. FRIEDMAN · 2021 to 2026
$2.6M
The Cell and Molecular Biology of Myofibroblasts in Hepatic FibrosisR01DK098819 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI ROCKEY, DON C. · 2014 to 2017
$1.3M
Hepatic autophagy, progenitor cells and fibrosisR56DK056621 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI FRIEDMAN, SCOTT L. · 2015 to 2015
$297k
NIDDK NIH HHS P30 DK123704NIDDK NIH HHS R01 DK056621NIDDK NIH HHS R01 DK057830NIDDK NIH HHS R01 DK098819NIDDK NIH HHS R01 DK113159NIDDK NIH HHS R01 DK128289NIDDK NIH HHS R56 DK056621NIGMS NIH HHS P20 GM130457
6 · The paper itself

Abstract

Hepatitis C virus (HCV) infection and its complications have been the major cause of cirrhosis and its complications for several decades in the Western world. Until recently, treatment for HCV with interferon-based regimens was associated with moderate success but was difficult to tolerate. More recently, however, an arsenal of novel and highly effective direct-acting antiviral (DAA) drugs has transformed the landscape by curing HCV in a broad range of patients, including those with established advanced fibrosis, cirrhosis, comorbidities, and even those with complications of cirrhosis. Fibrosis is a dynamic process comprising both extracellular matrix deposition, as well as its degradation. With almost universal sustained virologic response (SVR) (ie, elimination of HCV), it is timely to explore whether HCV eradication can reverse fibrosis and cirrhosis. Indeed, fibrosis in several types of liver disease is reversible, including HCV. However, we do not know with certainty in whom fibrosis regression can be expected after HCV elimination, how quickly it occurs, and whether antifibrotic therapies will be indicated in those with persistent cirrhosis. This review summarizes the evidence for reversibility of fibrosis and cirrhosis after HCV eradication, its impact on clinical outcomes, and therapeutic prospects for directly promoting fibrosis regression in patients whose fibrosis persists after SVR.

Indexed as

Translational Research, BiomedicalAnimalsAntiviral AgentsHepacivirusHepatitis CHost-Pathogen InteractionsHumansLiverLiver CirrhosisLiver RegenerationRemission InductionTreatment OutcomeAntiviral AgentsDirect-Acting AntiviralFibrosis RegressionHepatitis C VirusSustained Virologic Response

Identifiers

PMID33529675
PMCPMC8601597
OpenAlexW3127821066

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.