Evidence map›Paper›PMID 30142879›Full record

ReviewInternational journal of molecular sciences2018

Roles of the TGF-β⁻VEGF-C Pathway in Fibrosis-Related Lymphangiogenesis.

Hiroshi Kinashi, Yasuhiko Ito, Ting Sun, Takayuki Katsuno, Yoshifumi Takei

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 2 pooled it
2.6field-weighted citation impact, top 7% 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

51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 85 citations in OpenAlex.

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  20. Angiogenesis-An Emerging Role in Organ Fibrosis.International journal of molecular sciences · 2023
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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

5 authors at 3 institutions in 1 country.

Hiroshi KinashiDepartment of Nephrology and Rheumatology, Aichi Medical University, Nagakute 480-1195, Japan. hiroshi.kinashi@gmail.com.
Yasuhiko ItoDepartment of Nephrology and Rheumatology, Aichi Medical University, Nagakute 480-1195, Japan. yasuito@aichi-med-u.ac.jp.
Ting SunDepartment of Nephrology and Renal Replacement Therapy, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan. tinasuen1991@gmail.com.
Takayuki KatsunoDepartment of Nephrology and Rheumatology, Aichi Medical University, Nagakute 480-1195, Japan. t-katsuno@aichi-med-u.ac.jp.
Yoshifumi TakeiDepartment of Medicinal Biochemistry, School of Pharmacy, Aichi Gakuin University, Nagoya 464-8650, Japan. takei@dpc.agu.ac.jp.
Aichi Medical University · JPAichi Gakuin University · JPNagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lymphatic vessels drain excess tissue fluids to maintain the interstitial environment. Lymphatic capillaries develop during the progression of tissue fibrosis in various clinical and pathological situations, such as chronic kidney disease, peritoneal injury during peritoneal dialysis, tissue inflammation, and tumor progression. The role of fibrosis-related lymphangiogenesis appears to vary based on organ specificity and etiology. Signaling via vascular endothelial growth factor (VEGF)-C, VEGF-D, and VEGF receptor (VEGFR)-3 is a central molecular mechanism for lymphangiogenesis. Transforming growth factor-β (TGF-β) is a key player in tissue fibrosis. TGF-β induces peritoneal fibrosis in association with peritoneal dialysis, and also induces peritoneal neoangiogenesis through interaction with VEGF-A. On the other hand, TGF-β has a direct inhibitory effect on lymphatic endothelial cell growth. We proposed a possible mechanism of the TGF-β⁻VEGF-C pathway in which TGF-β promotes VEGF-C production in tubular epithelial cells, macrophages, and mesothelial cells, leading to lymphangiogenesis in renal and peritoneal fibrosis. Connective tissue growth factor (CTGF) is also involved in fibrosis-associated renal lymphangiogenesis through interaction with VEGF-C, in part by mediating TGF-β signaling. Further clarification of the mechanism might lead to the development of new therapeutic strategies to treat fibrotic diseases.

Indexed as

AnimalsConnective Tissue Growth FactorEpithelial CellsGene Expression RegulationHumansLymphangiogenesisLymphatic VesselsMacrophagesNephrogenic Fibrosing DermopathyPeritoneal FibrosisRenal Insufficiency, ChronicSignal TransductionTransforming Growth Factor betaVascular Endothelial Growth Factor CVascular Endothelial Growth Factor DVascular Endothelial Growth Factor Receptor-3CCN2 protein, humanConnective Tissue Growth FactorFLT4 protein, humanTransforming Growth Factor betaVascular Endothelial Growth Factor CVascular Endothelial Growth Factor DVascular Endothelial Growth Factor Receptor-3fibrosislymphangiogenesistransforming growth factor-βvascular endothelial growth factor-C

Identifiers

PMID30142879
PMCPMC6163754
OpenAlexW2888262430

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.