Evidence map›Paper›PMID 34923653›Full record

ReviewHepatology (Baltimore, Md.)2022

Hepatic fibrosis 2022: Unmet needs and a blueprint for the future.

Scott L Friedman, Massimo Pinzani

Abstract readReview
In one paragraph

Review in Hepatology (Baltimore, Md.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 221 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
221citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

221 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Noninvasive Evaluation of Prolonged-Release Pirfenidone in Compensated Liver Cirrhosis. ODISEA Study, a Randomised Trial.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Trial
  5. Trial
  6. On the History of Hepatic Vein Catheterization.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Review
  7. Review
  8. Review
  9. Gut-Derived Sodium Butyrate Attenuates Liver Fibrosis by Inhibiting Aerobic Glycolysis via the HDAC3/c-Myc Signaling Axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  10. Therapeutics for Alcohol-Associated Liver Disease.Annual review of pharmacology and toxicology · 2026
    Review
  11. Article
  12. Reprogramming macrophages to treat liver diseases.Hepatology (Baltimore, Md.) · 2026
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

161 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.

Scott L FriedmanDivision of Liver DiseasesIcahn School of Medicine at Mount SinaiNew YorkNew YorkUSA.ORCID 0000-0003-1178-6195
Massimo PinzaniInstitute for Liver and Digestive HealthUniversity College LondonLondonUK.

Funding

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
NIDDK NIH HHS 1 R01 DK128289-01NIDDK NIH HHS R01 DK128289
6 · The paper itself

Abstract

Steady progress over four decades toward understanding the pathogenesis and clinical consequences of hepatic fibrosis has led to the expectation of effective antifibrotic drugs, yet none has been approved. Thus, an assessment of the field is timely, to clarify priorities and accelerate progress. Here, we highlight the successes to date but, more importantly, identify gaps and unmet needs, both experimentally and clinically. These include the need to better define cell-cell interactions and etiology-specific elements of fibrogenesis and their link to disease-specific drivers of portal hypertension. Success in treating viral hepatitis has revealed the remarkable capacity of the liver to degrade scar in reversing fibrosis, yet we know little of the mechanisms underlying this response. Thus, there is an exigent need to clarify the cellular and molecular mechanisms of fibrosis regression in order for therapeutics to mimic the liver's endogenous capacity. Better refined and more predictive in vitro and animal models will hasten drug development. From a clinical perspective, current diagnostics are improving but not always biologically plausible or sufficiently accurate to supplant biopsy. More urgently, digital pathology methods that leverage machine learning and artificial intelligence must be validated in order to capture more prognostic information from liver biopsies and better quantify the response to therapies. For more refined treatment of NASH, orthogonal approaches that integrate genetic, clinical, and pathological data sets may yield treatments for specific subphenotypes of the disease. Collectively, these and other advances will strengthen and streamline clinical trials and better link histologic responses to clinical outcomes.

Indexed as

Antifibrotic AgentsAnimalsBiomedical ResearchClinical Trials as TopicDrug DevelopmentFibrosisHumansLiverLiver CirrhosisNeeds AssessmentAntifibrotic Agents

Identifiers

PMID34923653
PMCPMC12179971

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.