Evidence map›Paper›PMID 32880077›Full record

ReviewHepatology international2020

The role of neutrophils in innate immunity-driven nonalcoholic steatohepatitis: lessons learned and future promise.

Lihong Wu, Xiang Gao, Qianyu Guo, Jufei Li, Jianyu Yao, Kaixuan Yan, Ying Xu, Xue Jiang, Dewei Ye, Jiao Guo

Abstract readReview
PubMed Publisher
In one paragraph

Review in Hepatology international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 9% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Molecular mechanisms in MASLD/MASH-related HCC.Hepatology (Baltimore, Md.) · 2025
    Review
  8. HFD Exacerbates Hepatic Lipid Metabolism Disorders After Cholecystectomy by Regulating the Bile Acid and Neutrophil Recruitment.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
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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

10 authors at 1 institution in 1 country.

Lihong WuKey Laboratory of Glucolipid Metabolic Diseases of the Ministry of Education, Guangzhou Higher Education Mega, Guangdong Pharmaceutical University, Lab 406, 4th Floor, Science and Technology Building, 280 Waihuan East Road, Guangzhou, China.
Xiang GaoKey Laboratory of Glucolipid Metabolic Diseases of the Ministry of Education, Guangzhou Higher Education Mega, Guangdong Pharmaceutical University, Lab 406, 4th Floor, Science and Technology Building, 280 Waihuan East Road, Guangzhou, China.
Qianyu GuoKey Laboratory of Glucolipid Metabolic Diseases of the Ministry of Education, Guangzhou Higher Education Mega, Guangdong Pharmaceutical University, Lab 406, 4th Floor, Science and Technology Building, 280 Waihuan East Road, Guangzhou, China.
Jufei LiKey Laboratory of Glucolipid Metabolic Diseases of the Ministry of Education, Guangzhou Higher Education Mega, Guangdong Pharmaceutical University, Lab 406, 4th Floor, Science and Technology Building, 280 Waihuan East Road, Guangzhou, China.
Jianyu YaoKey Laboratory of Glucolipid Metabolic Diseases of the Ministry of Education, Guangzhou Higher Education Mega, Guangdong Pharmaceutical University, Lab 406, 4th Floor, Science and Technology Building, 280 Waihuan East Road, Guangzhou, China.
Kaixuan YanKey Laboratory of Glucolipid Metabolic Diseases of the Ministry of Education, Guangzhou Higher Education Mega, Guangdong Pharmaceutical University, Lab 406, 4th Floor, Science and Technology Building, 280 Waihuan East Road, Guangzhou, China.
Ying XuThe First Affiliated Hospital/School of Clinical Medicine, Guangdong Pharmaceutical University, Guangzhou, China.
Xue JiangKey Laboratory of Glucolipid Metabolic Diseases of the Ministry of Education, Guangzhou Higher Education Mega, Guangdong Pharmaceutical University, Lab 406, 4th Floor, Science and Technology Building, 280 Waihuan East Road, Guangzhou, China.
Dewei YeKey Laboratory of Glucolipid Metabolic Diseases of the Ministry of Education, Guangzhou Higher Education Mega, Guangdong Pharmaceutical University, Lab 406, 4th Floor, Science and Technology Building, 280 Waihuan East Road, Guangzhou, China. deweiye@gdpu.edu.cn.ORCID http://orcid.org/0000-0003-1295-3063
Jiao GuoKey Laboratory of Glucolipid Metabolic Diseases of the Ministry of Education, Guangzhou Higher Education Mega, Guangdong Pharmaceutical University, Lab 406, 4th Floor, Science and Technology Building, 280 Waihuan East Road, Guangzhou, China. gyguoyz@163.com.
Guangdong Pharmaceutical University · CN

Funding

Key Research Program in Department of Education of Guangdong Province 2016KZDXM041NSFC Grant, China 81570701NSFC Grant, China 81770849Research Fund in TCM Bureau of Guangdong Province 20181156
6 · The paper itself

Abstract

The enrichment of innate immune cells and the enhanced inflammation represent the hallmark of non-alcoholic steatohepatitis (NASH), the advanced subtype with a significantly increased risk of progression to end-stage liver diseases within the spectrum of non-alcoholic fatty liver disease. Neutrophils are traditionally recognized as key components in the innate immune system to defend against pathogens. Recently, a growing body of evidence supports neutrophils as emerging key player in mediating the transition from steatosis to NASH, which is largely inspired by the histological findings in human liver biopsy indicating the enhanced infiltration of neutrophils as one of the key histological features of NASH. In this review, we discuss data regarding histological perspectives of hepatic infiltration of neutrophils in NASH. We also highlight the pathophysiological role of neutrophils in promoting metabolic inflammation in the liver through the release of a vast array of granule proteins, the interaction with other pro-inflammatory immune cells, and the formation of neutrophil extracellular traps. Neutrophil granule proteins possess pleiotropic effects on regulating neutrophil biology and functions. A variety of granule proteins (including lipocalin-2, myeloperoxidase, proteinase 3, neutrophil elastase, etc.) produced by neutrophils enhance liver metabolic inflammation, thereby promoting NASH progression by mediating neutrophil-macrophage interaction. Therapeutically, pharmacological inhibitors targeting neutrophil granule proteins hold promise to combat NASH. In addition, this article also summarizes potentials of neutrophils and its derived various granule proteins for the accurate, even non-invasive diagnosis of NASH.

Indexed as

LiverNeutrophil InfiltrationNeutrophilsNon-alcoholic Fatty Liver DiseaseBiomarkersHumansImmunity, InnateBiomarkersBiomarkersFatty liverInnate immunityLiver inflammationMacrophagesNASHNeutrophil extracellular trapsNeutrophil granule proteinsNeutrophil-macrophage axisSerine protease

Identifiers

PMID32880077
OpenAlexW3082706973

What OpenQuestion holds

Textmetadata
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.