Evidence map›Paper›PMID 32258944›Full record

ReviewHepatology communications2020

Pathogenesis of Nonalcoholic Steatohepatitis: An Overview.

Gopanandan Parthasarathy, Xavier Revelo, Harmeet Malhi

Open access · goldAbstract readReview
In one paragraph

Review in Hepatology communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 231 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
231citing papers in PubMed, 4 pooled it
38.8field-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

231 citing papers in PubMed, 4 syntheses or guidelines pooled it, 416 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Fermented Milk as an Alternative Therapy for Obesity.International journal of food science · 2026
    Review
  12. Frontiers in medicine · 2026
    Review
  13. Review
  14. Article
  15. The Paraoxonase (International journal of molecular sciences · 2025
    Review
  16. Article
  17. Effects of sodium-glucose cotransporter 2 inhibitors in patients with type 2 diabetes and nonalcoholic fatty liver disease: A cohort study.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2025
    Article
  18. World journal of hepatology · 2025
    Article
  19. Review
  20. Review

171 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

3 authors at 2 institutions in 1 country.

Gopanandan ParthasarathyDivision of Gastroenterology and Hepatology Mayo Clinic Rochester MN.
Xavier ReveloDepartment of Integrative Biology and Physiology University of Minnesota Minneapolis MN.ORCID https://orcid.org/0000-0002-2754-509X
Harmeet MalhiDivision of Gastroenterology and Hepatology Mayo Clinic Rochester MN.ORCID https://orcid.org/0000-0002-0882-4990
Mayo Clinic in Arizona · USUniversity of Minnesota · US

Funding

Pathobiology of Liver InjuryR01DK111378 · NIDDK · MAYO CLINIC ROCHESTER · PI MALHI, HARMEET · 2016 to 2025
$3.9M
Mechanisms of B Cell Pathogenicity in Non-Alcoholic Fatty Liver DiseaseR01DK122056 · NIDDK · UNIVERSITY OF MINNESOTA · PI REVELO, XAVIER · 2019 to 2023
$1.7M
NIDDK NIH HHS R01 DK111378NIDDK NIH HHS R01 DK122056
6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) is a heterogeneous group of liver diseases characterized by the accumulation of fat in the liver. The heterogeneity of NAFLD is reflected in a clinical and histologic spectrum where some patients develop isolated steatosis of the liver, termed nonalcoholic fatty liver, whereas others develop hepatocyte injury, ballooning, inflammation, and consequent fibrosis, termed nonalcoholic steatohepatitis (NASH). Systemic insulin resistance is a major driver of hepatic steatosis in NAFLD. Lipotoxicity of accumulated lipids along with activation of the innate immune system are major drivers of NASH. Lipid-induced sublethal and lethal stress culminates in the activation of inflammatory processes, such as the release of proinflammatory extracellular vesicles and cell death. Innate and adaptive immune mechanisms involving macrophages, dendritic cells, and lymphocytes are central drivers of inflammation that recognize damage- and pathogen-associated molecular patterns and contribute to the progression of the inflammatory cascade. While the activation of the innate immune system and the recruitment of proinflammatory monocytes into the liver in NASH are well known, the exact signals that lead to this remain less well defined. Further, the contribution of other immune cell types, such as neutrophils and B cells, is an area of intense research. Many host factors, such as the microbiome and gut-liver axis, modify individual susceptibility to NASH. In this review, we discuss lipotoxicity, inflammation, and the contribution of interorgan crosstalk in NASH pathogenesis.

Identifiers

PMID32258944
PMCPMC7109346
OpenAlexW2999907367

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.