Evidence map›Paper›PMID 24779927›Full record

ArticleJournal of cellular and molecular medicine2014

Curcumin attenuates angiogenesis in liver fibrosis and inhibits angiogenic properties of hepatic stellate cells.

Feng Zhang, Zili Zhang, Li Chen, Desong Kong, Xiaoping Zhang, Chunfeng Lu, Yin Lu, Shizhong Zheng

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
8.0field-weighted citation impact, top 2% 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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Curcumin in Fibrosis Treatment: A Review.Drug design, development and therapy · 2026
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  7. Article
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  11. Curcumin Inhibits Oxidative Stress and Apoptosis Induced by HAnimals : an open access journal from MDPI · 2024
    Article
  12. Article
  13. Review
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  16. 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

8 authors at 1 institution in 1 country.

Feng ZhangDepartment of Pharmacology, College of Pharmacy, Nanjing University of Chinese Medicine, Nanjing, China.
Zili Zhang
Li Chen
Desong Kong
Xiaoping Zhang
Chunfeng Lu
Yin Lu
Shizhong Zheng
Nanjing University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatic fibrosis is concomitant with sinusoidal pathological angiogenesis, which has been highlighted as novel therapeutic targets for the treatment of chronic liver disease. Our prior studies have demonstrated that curcumin has potent antifibrotic activity, but the mechanisms remain to be elucidated. The current work demonstrated that curcumin ameliorated fibrotic injury and sinusoidal angiogenesis in rat liver with fibrosis caused by carbon tetrachloride. Curcumin reduced the expression of a number of angiogenic markers in fibrotic liver. Experiments in vitro showed that the viability and vascularization of rat liver sinusoidal endothelial cells and rat aortic ring angiogenesis were not impaired by curcumin. These results indicated that hepatic stellate cells (HSCs) that are characterized as liver-specific pericytes could be potential target cells for curcumin. Further investigations showed that curcumin inhibited VEGF expression in HSCs associated with disrupting platelet-derived growth factor-β receptor (PDGF-βR)/ERK and mTOR pathways. HSC motility and vascularization were also suppressed by curcumin associated with blocking PDGF-βR/focal adhesion kinase/RhoA cascade. Gain- or loss-of-function analyses revealed that activation of peroxisome proliferator-activated receptor-γ (PPAR-γ) was required for curcumin to inhibit angiogenic properties of HSCs. We concluded that curcumin attenuated sinusoidal angiogenesis in liver fibrosis possibly by targeting HSCs via a PPAR-γ activation-dependent mechanism. PPAR-γ could be a target molecule for reducing pathological angiogenesis during liver fibrosis.

Indexed as

AnimalsAntineoplastic AgentsApoptosisBlotting, WesternCarbon TetrachlorideCell ProliferationCells, CulturedCurcuminEnzyme-Linked Immunosorbent AssayFluorescent Antibody TechniqueHepatic Stellate CellsLiver CirrhosisMaleNeovascularization, PathologicRatsRats, Sprague-DawleyAntineoplastic AgentsCarbon TetrachlorideCurcuminRNA, Messengerangiogenesiscurcuminhepatic stellate cellliver fibrosisperoxisome proliferator-activated receptor-γVEGF

Identifiers

PMID24779927
PMCPMC4124023
OpenAlexW2034015019

What OpenQuestion holds

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LicenceCC BY
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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.