Evidence map›Paper›PMID 30588181›Full record

ReviewInternational journal of medical sciences2018

Phenotypic Alteration of Hepatocytes in Non-Alcoholic Fatty Liver Disease.

Hari Vishal Lakhani, Dana Sharma, Michael W Dodrill, Athar Nawab, Nitin Sharma, Cameron Lee Cottrill, Joseph I Shapiro, Komal Sodhi

Open access · goldAbstract readReview
In one paragraph

Review in International journal of medical sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 48 citations in OpenAlex.

  1. Mechanical interplay between adipose tissues and disease progression.Bioengineering & translational medicine · 2026
    Review
  2. Review
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  5. International journal of molecular sciences · 2024
    Article
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  7. Article
  8. Review
  9. Article
  10. Review
  11. Cellular heterogeneity and plasticity during NAFLD progression.Frontiers in molecular biosciences · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
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  18. Review
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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

8 authors at 1 institution in 1 country.

Hari Vishal LakhaniDepartment of Internal Medicine, Marshall University Joan C Edwards School of Medicine, Huntington, WV, USA.
Dana SharmaDepartment of Internal Medicine, Marshall University Joan C Edwards School of Medicine, Huntington, WV, USA.
Michael W DodrillDepartment of Internal Medicine, Marshall University Joan C Edwards School of Medicine, Huntington, WV, USA.
Athar NawabDepartment of Internal Medicine, Marshall University Joan C Edwards School of Medicine, Huntington, WV, USA.
Nitin SharmaDepartment of Internal Medicine, Marshall University Joan C Edwards School of Medicine, Huntington, WV, USA.
Cameron Lee CottrillDepartment of Internal Medicine, Marshall University Joan C Edwards School of Medicine, Huntington, WV, USA.
Joseph I ShapiroDepartment of Internal Medicine, Marshall University Joan C Edwards School of Medicine, Huntington, WV, USA.
Komal SodhiDepartment of Surgery, Marshall University Joan C Edwards School of Medicine, Huntington, WV, USA.
Marshall University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-Alcoholic Fatty Liver Disease (NAFLD) has been recognized as the most common liver disorder in developed countries. NAFLD progresses from fat accumulation in hepatocytes to steatohepatitis to further stages of fibrosis and cirrhosis. Simple steatosis, i.e. fat deposition in the liver, is considered benign and gives way to non-alcoholic steatohepatitis (NASH) with a higher probability of progressing to cirrhosis, and liver-related mortality. Evidence has been found that this progression has been associated with marked alterations in hepatocyte histology and a shift in marker expression of healthy hepatocytes including increased expression of peroxisome proliferator-activated receptor gamma (PPARγ), adipocyte protein (aP2), CD36, interleukin-6 (IL-6), interleukin-18 (IL-18) and adiponectin. This progression shares much in common with the obesity phenotype, which involves a transformation of adipocytes from small, healthy cells to large, dysfunctional ones that contribute to redox imbalance and the progression of metabolic syndrome. Further, activation of Src/ERK signaling via the sodium potassium adenosine triphosphatase (Na/K-ATPase) α-1 subunit in impaired hepatocytes may contribute to redox imbalance, exacerbating the progression of NAFLD. This review hypothesizes that an adipogenic transformation of hepatocytes propagates redox imbalance and that the processes occurring in adipogenesis become activated in fat-laden hepatocytes in liver, thereby driving progression to NAFLD. Further, this review discusses therapeutic interventions to reverse NAFLD including the thiazolidinediones (TZDs) and a variety of antioxidant species. The peptide, pNaKtide, which is an antagonist of Na/K-ATPase signaling, is also proposed as a potential pharmacologic option for reducing reactive oxygen species (ROS) and reversing NAFLD by inhibiting the Na/K-ATPase-modulated ROS amplification loop.

Indexed as

AdipogenesisAnimalsAntioxidantsBiomarkersDisease Models, AnimalDisease ProgressionHepatocytesHumansLiverLiver CirrhosisMAP Kinase Signaling SystemNon-alcoholic Fatty Liver DiseaseOxidative StressReactive Oxygen SpeciesSodium-Potassium-Exchanging ATPaseThiazolidinedionesAntioxidantsBiomarkersReactive Oxygen SpeciesSodium-Potassium-Exchanging ATPaseThiazolidinedionesHepatocytesNon-Alcoholic Fatty Liver Disease

Identifiers

PMID30588181
PMCPMC6299410
OpenAlexW2898188130

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.