Evidence map›Paper›PMID 26028039›Full record

ReviewCurrent drug targets2015

IL-17 Axis Driven Inflammation in Non-Alcoholic Fatty Liver Disease Progression.

Daniel A Giles, Maria E Moreno-Fernandez, Senad Divanovic

Open access · greenAbstract readReview
In one paragraph

Review in Current drug targets, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 6% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Molecular mechanisms in MASLD/MASH-related HCC.Hepatology (Baltimore, Md.) · 2025
    Review
  10. Review
  11. The Association BetweenNutrients · 2025
    Article
  12. cPLACytotechnology · 2025
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Interleukins in liver disease treatment.World journal of hepatology · 2024
    Article
  19. Article
  20. Article

1 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 1 institution in 1 country.

Daniel A Giles
Maria E Moreno-Fernandez
Senad DivanovicDivision of Immunobiology Cincinnati Children's Hospital Medical Center TCHRF - Location S, Room #S.5.409 3333 Burnet Avenue Cincinnati, Ohio 45229-3039 U.S.A. senad.divanovic@cchmc.org.
Cincinnati Children's Hospital Medical Center · US

Funding

Immunopathogenesis of Non-alcoholic Fatty Liver DiseaseR01DK099222 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Senad Divanovic · 2013 to 2026
$5.6M
NIDDK NIH HHS R01 DK099222NIDDK NIH HHS R01DK099222NIDDK NIH HHS R01DK099222-S1
6 · The paper itself

Abstract

Obesity is a primary risk factor for the development of non-alcoholic fatty liver disease (NAFLD). NAFLD, the most common chronic liver disease in the world, represents a spectrum of disorders that range from steatosis (NAFL) to steatohepatitis (NASH) to cirrhosis. It is anticipated that NAFLD will soon surpass chronic hepatitis C infection as the leading cause for needing liver transplantation. Despite its clinical and public health significance no specific therapies are available. Although the etiology of NAFLD is multifactorial and remains largely enigmatic, it is well accepted that inflammation is a central component of NAFLD pathogenesis. Despite the significance, critical immune mediators, loci of immune activation, the immune signaling pathways and the mechanism(s) underlying disease progression remain incompletely understood. Recent findings have focused on the role of Interleukin 17 (IL-17) family of proinflammatory cytokines in obesity and pathogenesis of obesity-associated sequelae. Notably, obesity favors a Th17 bias and is associated with increased IL-17A expression in both humans and mice. Further, in mice, IL-17 axis has been implicated in regulation of both obesity and NAFLD pathogenesis. However, despite these recent advances several important questions require further evaluation including: the relevant cellular source of IL-17A production; the critical IL- 17RA-expressing cell type; the critical liver infiltrating immune cells; and the underlying cellular effector mechanisms. Addressing these questions may aid in the identification and development of novel therapeutic targets for prevention of inflammation- driven NAFLD progression.

Indexed as

AnimalsDisease ProgressionHumansInflammationInterleukin-17LiverMiceNon-alcoholic Fatty Liver DiseaseObesityInterleukin-17

Identifiers

PMID26028039
PMCPMC4929857
OpenAlexW659490281

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.