Evidence map›Paper›PMID 38414375›Full record

ReviewClinical and molecular hepatology2024

Liver sinusoidal endothelial cell: An important yet often overlooked player in the liver fibrosis.

Jiaorong Qu, Le Wang, Yufei Li, Xiaojiaoyang Li

Open access · goldAbstract readReview
In one paragraph

Review in Clinical and molecular hepatology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
16.6field-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

48 citing papers in PubMed, 45 citations in OpenAlex.

  1. Identification of Prognostic Factors and Regulatory Pathways in Porto-Sinusoidal Vascular Disorder.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Article
  2. Article
  3. E3 Ubiquitin Ligases in MASH-Associated Liver Fibrosis: Mechanisms and Therapeutic Opportunities.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Review
  4. Article
  5. Autophagy in MASLD: A Metabolic and Precision Medicine Perspective.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Review
  6. Precision pathophysiology in steatotic liver disease.Clinical and molecular hepatology · 2026
    Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Kupffer cells: Orchestrators of liver physiology.Liver research (Beijing, China) · 2026
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Jiaorong QuSchool of Life Sciences, Beijing University of Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China.
Le WangSchool of Life Sciences, Beijing University of Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China.
Yufei LiSchool of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, China.
Xiaojiaoyang LiSchool of Life Sciences, Beijing University of Chinese Medicine, Beijing University of Chinese Medicine, Beijing, China.
Beijing University of Chinese Medicine · CN

Funding

National High-Level Talents Special Support ProgramNational Key Research and Development Program on Modernization of Traditional Chinese Medicine 2022YFC3502100National Natural Science Foundation of China 82274186
6 · The paper itself

Abstract

Liver sinusoidal endothelial cells (LSECs) are liver-specific endothelial cells with the highest permeability than other mammalian endothelial cells, characterized by the presence of fenestrae on their surface, the absence of diaphragms and the lack of basement membrane. Located at the interface between blood and other liver cell types, LSECs mediate the exchange of substances between the blood and the Disse space, playing a crucial role in maintaining substance circulation and homeostasis of multicellular communication. As the initial responders to chronic liver injury, the abnormal LSEC activation not only changes their own physicochemical properties but also interrupts their communication with hepatic stellate cells and hepatocytes, which collectively aggravates the process of liver fibrosis. In this review, we have comprehensively updated the various pathways by which LSECs were involved in the initiation and aggravation of liver fibrosis, including but not limited to cellular phenotypic change, the induction of capillarization, decreased permeability and regulation of intercellular communications. Additionally, the intervention effects and latest regulatory mechanisms of anti-fibrotic drugs involved in each aspect have been summarized and discussed systematically. As we studied deeper into unraveling the intricate role of LSECs in the pathophysiology of liver fibrosis, we unveil a promising horizon that pave the way for enhanced patient outcomes.

Indexed as

Endothelial CellsLiverLiver CirrhosisAnimalsCell CommunicationHepatic Stellate CellsHepatocytesHumansCapillarizationFenestraeIntercellular communicationLiver fibrosisLiver sinusoidal endothelial cells

Identifiers

PMID38414375
PMCPMC11261236
OpenAlexW4392237798

What OpenQuestion holds

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LicenceCC BY-NC
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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.