Evidence map›Paper›PMID 29368124›Full record

ReviewDigestive diseases and sciences2018

Origins of Portal Hypertension in Nonalcoholic Fatty Liver Disease.

Gyorgy Baffy

Registry-linked trialOpen access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Digestive diseases and sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04191044 (Portal Hypertension in Non-alcoholic Fatty Liver Disease), which is not on this map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.7field-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.

NCT04191044 unknown statusnot on this mapstarted 2020, after this paper: background citation

Portal Hypertension in Non-alcoholic Fatty Liver Disease: Association With Cardiovascular Risk and Identification of Non-invasive Biomarkers

TypeobservationalSponsorInstituto de Investigación Marqués de ValdecillaRan2020 to 2020Enrolled170ConditionsFatty Liver DiseaseArmsA complete cardiovascular and liver characterization will be carried out
3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
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  6. Review
  7. Article
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  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Mechanobiology of portal hypertension.JHEP reports : innovation in hepatology · 2023
    Review
  15. Portal Hypertension in Nonalcoholic Fatty Liver Disease: Challenges and Paradigms.Journal of clinical and translational hepatology · 2023
    Review
  16. Article
  17. Review
  18. Review
  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

1 author at 1 institution in 1 country.

Gyorgy BaffyDepartment of Medicine, VA Boston Healthcare System and Brigham and Women's Hospital, Harvard Medical School, 150 South Huntington Avenue, Room 6A-46, Boston, MA, 02130, USA. gbaffy@bwh.harvard.edu.ORCID http://orcid.org/0000-0002-8334-0400
Brigham and Women's Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nonalcoholic fatty liver disease (NAFLD) advanced to cirrhosis is often complicated by clinically significant portal hypertension, which is primarily caused by increased intrahepatic vascular resistance. Liver fibrosis has been identified as a critical determinant of this process. However, there is evidence that portal venous pressure may begin to rise in the earliest stages of NAFLD when fibrosis is far less advanced or absent. The biological and clinical significance of these early changes in sinusoidal homeostasis remains unclear. Experimental and human observations indicate that sinusoidal space restriction due to hepatocellular lipid accumulation and ballooning may impair sinusoidal flow and generate shear stress, increasingly disrupting sinusoidal microcirculation. Sinusoidal endothelial cells, hepatic stellate cells, and Kupffer cells are key partners of hepatocytes affected by NAFLD in promoting endothelial dysfunction through enhanced contractility, capillarization, adhesion and entrapment of blood cells, extracellular matrix deposition, and neovascularization. These biomechanical and rheological changes are aggravated by a dysfunctional gut-liver axis and splanchnic vasoregulation, culminating in fibrosis and clinically significant portal hypertension. We may speculate that increased portal venous pressure is an essential element of the pathogenesis across the entire spectrum of NAFLD. Improved methods of noninvasive portal venous pressure monitoring will hopefully give new insights into the pathobiology of NAFLD and help efforts to identify patients at increased risk for adverse outcomes. In addition, novel drug candidates targeting reversible components of aberrant sinusoidal circulation may prevent progression in NAFLD.

Indexed as

HumansHypertension, PortalNon-alcoholic Fatty Liver DiseaseEndothelial dysfunctionHepatic venous pressure gradientIntrahepatic vascular resistanceSinusoidal homeostasis

Identifiers

PMID29368124
OpenAlexW2784792741

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

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 Socratic graph.