Evidence map›Paper›PMID 34280515›Full record

ReviewAdvanced drug delivery reviews2021

Pathophysiological communication between hepatocytes and non-parenchymal cells in liver injury from NAFLD to liver fibrosis.

Santosh Kumar, Qihua Duan, Rongxue Wu, Edward N Harris, Qiaozhu Su

Open access · greenAbstract readReview
In one paragraph

Review in Advanced drug delivery reviews, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 196 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
196citing papers in PubMed, 4 pooled it
29.8field-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

196 citing papers in PubMed, 4 syntheses or guidelines pooled it, 319 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Gut microbes · 2026
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  15. Article
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  17. Review
  18. Article
  19. Selenium and Liver Steatosis and Fibrosis: Opposing Direct and Steatosis-Mediated Associations in a Large Cohort.JGH open : an open access journal of gastroenterology and hepatology · 2026
    Article
  20. Article

136 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

5 authors at 3 institutions in 2 countries.

Santosh KumarInstitute for Global Food Security, School of Biological Sciences, Queen's University Belfast, Belfast BT9 5DL, United Kingdom.
Qihua DuanInstitute for Global Food Security, School of Biological Sciences, Queen's University Belfast, Belfast BT9 5DL, United Kingdom.
Rongxue WuDepartment of Medicine, Section of Cardiology, University of Chicago, Chicago, USA.
Edward N HarrisDepartment of Biochemistry, University of Nebraska-Lincoln, Lincoln, NE 68588, USA. Electronic address: eharris5@unl.edu.
Qiaozhu SuInstitute for Global Food Security, School of Biological Sciences, Queen's University Belfast, Belfast BT9 5DL, United Kingdom. Electronic address: q.su@qub.ac.uk.
Queen's University Belfast · GBUniversity of Chicago · USUniversity of Nebraska–Lincoln · US

Funding

Liver-Mediated Clearance of Low Molecular Weight HeparinsR01HL130864 · NHLBI · UNIVERSITY OF NEBRASKA LINCOLN · PI HARRIS, EDWARD N · 2016 to 2019
$1.6M
British Heart Foundation PG/19/86134788British Heart Foundation PG/19/86/34788NHLBI NIH HHS R01 HL130864
6 · The paper itself

Abstract

Non-alcoholic fatty liver disease (NAFLD) is a multifactorial disease that encompasses a spectrum of pathological conditions, ranging from simple steatosis (NAFL), nonalcoholic steatohepatitis (NASH), fibrosis/cirrhosis which can further progress to hepatocellular carcinoma and liver failure. The progression of NAFL to NASH and liver fibrosis is closely associated with a series of liver injury resulting from lipotoxicity, oxidative stress, redox imbalance (excessive nitric oxide), ER stress, inflammation and apoptosis that occur sequentially in different liver cells which ultimately leads to the activation of liver regeneration and fibrogenesis, augmenting collagen and extracellular matrix deposition and promoting liver fibrosis and cirrhosis. Type 2 diabetes is a significant risk factor in NAFLD development by accelerating liver damage. Here, we overview recent findings from human study and animal models on the pathophysiological communication among hepatocytes (HCs), Kupffer cells (KCs), hepatic stellate cells (HSCs) and liver sinusoidal endothelial cells (LSECs) during the disease development. The mechanisms of crucial signaling pathways, including Toll-like receptor, TGFβ and hedgehog mediated hepatic injury are also discussed. We further highlight the potentials of precisely targeting hepatic individual cell-type using nanotechnology as therapeutic strategy for the treatment of NASH and liver fibrosis.

Indexed as

HepatocytesLiver CirrhosisNon-alcoholic Fatty Liver DiseaseAnimalsCell CommunicationEndoplasmic Reticulum StressHedgehog ProteinsHumansInsulin ResistanceOxidative StressToll-Like ReceptorsTransforming Growth Factor betaHedgehog ProteinsToll-Like ReceptorsTransforming Growth Factor betaER stressHedgehog and TGFβLipotoxicityLiver fibrosisMetabolic inflammationNAFLDNASHNitric oxideOxidative stressTLRs

Identifiers

PMID34280515
PMCPMC11792083
OpenAlexW3183166775

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.