Evidence map›Paper›PMID 37792957›Full record

ReviewScience translational medicine2023

Found in translation-Fibrosis in metabolic dysfunction-associated steatohepatitis (MASH).

Shuang Wang, Scott L Friedman

Open access · greenAbstract readReview
In one paragraph

Review in Science translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed, 1 pooled it
25.3field-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

83 citing papers in PubMed, 1 synthesis or guideline pooled it, 118 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Precision pathophysiology in steatotic liver disease.Clinical and molecular hepatology · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Mechanisms and therapeutic insights into MASH-associated fibrosis.Trends in endocrinology and metabolism: TEM · 2026
    Review
  17. Review
  18. Sex and gender differences in metabolic dysfunction-associated liver disease.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2026
    Review
  19. Article
  20. Article

23 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 1 institution in 1 country.

Shuang WangDivision of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.ORCID 0000-0001-5037-4316
Scott L FriedmanDivision of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.ORCID 0000-0003-1178-6195
Icahn School of Medicine at Mount Sinai · US

Funding

THE TISCH CANCER INSTITUTE - CANCER CENTER SUPPORT GRANTP30CA196521 · NCI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Ramon E Parsons · 2015 to 2026
$35.4M
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
Hepatic stellate cell plasticity and maladaptive fibrogenic memory in chronic liver diseaseR01DK136016 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Shuang Wang · 2023 to 2026
$2.3M
Mannose metabolism as a regulator of hepatic stellate cell activation and fibrosisR01DK121154 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CHU, JAIME C · 2020 to 2024
$2.3M
NCI NIH HHS P30 CA196521NIDDK NIH HHS R01 DK121154NIDDK NIH HHS R01 DK128289NIDDK NIH HHS R01 DK136016
6 · The paper itself

Abstract

Metabolic dysfunction-associated steatohepatitis (MASH) is a severe form of liver disease that poses a global health threat because of its potential to progress to advanced fibrosis, leading to cirrhosis and liver cancer. Recent advances in single-cell methodologies, refined disease models, and genetic and epigenetic insights have provided a nuanced understanding of MASH fibrogenesis, with substantial cellular heterogeneity in MASH livers providing potentially targetable cell-cell interactions and behavior. Unlike fibrogenesis, mechanisms underlying fibrosis regression in MASH are still inadequately understood, although antifibrotic targets have been recently identified. A refined antifibrotic treatment framework could lead to noninvasive assessment and targeted therapies that preserve hepatocellular function and restore the liver's architectural integrity.

Indexed as

Fatty LiverLiver NeoplasmsCell CommunicationHumansLiver Cirrhosis

Identifiers

PMID37792957
PMCPMC10671253
OpenAlexW4387330412

What OpenQuestion 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 OpenQuestion graph.