Evidence map›Paper›PMID 34940991›Full record

ArticleHepatology (Baltimore, Md.)2022

A strategy of vascular-targeted therapy for liver fibrosis.

Yuan Lin, Meng-Qi Dong, Zhi-Min Liu, Meng Xu, Zhi-Hao Huang, Hong-Juan Liu, Yi Gao, Wei-Jie Zhou

Open access · hybridAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
7.6field-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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Yin-Dan-Ping-Gan Capsule Mitigates CCLPharmaceuticals (Basel, Switzerland) · 2026
    Article
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  16. Article
  17. Liver fibrosis progression analyzed with AI predicts renal decline.JHEP reports : innovation in hepatology · 2025
    Article
  18. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Yuan LinDepartment of Pathology, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde Foshan), Foshan, China.
Meng-Qi DongState Key Laboratory of Organ Failure Research, Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Zhi-Min LiuState Key Laboratory of Organ Failure Research, Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Meng XuDepartment of General Surgery & Guangdong Provincial Key Laboratory of Precision Medicine for Gastrointestinal Tumor, Nanfang Hospital, First Clinical Medical College, Southern Medical University, Guangzhou, China.
Zhi-Hao HuangState Key Laboratory of Organ Failure Research, Department of Pathology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Hong-Juan LiuDepartment of Bioinformation, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Yi GaoGeneral Surgery Center, Department of Hepatobiliary Surgery II, Guangdong Provincial, Research Center for Artificial Organ and Tissue Engineering, Guangzhou Clinical Research and Transformation Center for Artificial Liver, Institute of Regenerative Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
Wei-Jie ZhouDepartment of Pathology, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde Foshan), Foshan, China.ORCID 0000-0002-0021-9454
Southern Medical University · CNThe First People's Hospital of Shunde · CNNanfang Hospital · CNZhujiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsNo effective treatments are available for liver fibrosis. Angiogenesis is deeply involved in liver fibrogenesis. However, current controversial results suggest it is difficult to treat liver fibrosis through vascular targeting. There are three different microvessels in liver: portal vessels, liver sinusoids, and central vessels. The changes and roles for each of the three different vessels during liver fibrogenesis are unclear. We propose that they play different roles during liver fibrogenesis, and a single vascular endothelial cell (EC) regulator is not enough to fully regulate these three vessels to treat liver fibrosis. Therefore, a combined regulation of multiple different EC regulatory signaling pathway may provide new strategies for the liver fibrosis therapy. Herein, we present a proof-of-concept strategy by combining the regulation of leukocyte cell-derived chemotaxin 2 (LECT2)/tyrosine kinase with immunoglobulin-like and epidermal growth factor-like domains 1 signaling with that of vascular endothelial growth factor (VEGF)/recombinant VEGF (rVEGF) signaling. APPROACH AND

resultsThe CCl

conclusionsLiver vascular changes occurred at very early stage of fibrogenesis. Different vessels play different roles in liver fibrosis. The combinational treatment of AAV9-LECT2-shRNA and bevacizumab could significantly improve the therapeutic effects on liver fibrosis.

Indexed as

Liver CirrhosisVascular Endothelial Growth Factor AAnimalsBevacizumabDisease Models, AnimalLiverMiceRNA, Small InterferingBevacizumabRNA, Small InterferingVascular Endothelial Growth Factor A

Identifiers

PMID34940991
PMCPMC9543235
OpenAlexW4200560098

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.