Evidence map›Paper›PMID 34705054›Full record

ArticleCellular and molecular life sciences : CMLS2021

Recombinant thrombomodulin domain 1 rescues pathological angiogenesis by inhibition of HIF-1α-VEGF pathway.

Yi-Hsun Huang, Cheng-Hsiang Kuo, I-Chen Peng, Yi-Sheng Chang, Sung-Huei Tseng, Edward M Conway, Hua-Lin Wu

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Microglial polarization in retinal neovascularization: Friend or foe?Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
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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

7 authors at 3 institutions in 2 countries.

Yi-Hsun HuangDepartment of Ophthalmology, College of Medicine, National Cheng Kung University Hospital, National Cheng Kung University, Tainan, Taiwan. jackhyh@gmail.com.ORCID http://orcid.org/0000-0002-4150-5481
Cheng-Hsiang KuoInternational Center for Wound Repair and Regeneration, National Cheng Kung University, Tainan, Taiwan.
I-Chen PengDepartment of Ophthalmology, College of Medicine, National Cheng Kung University Hospital, National Cheng Kung University, Tainan, Taiwan.
Yi-Sheng ChangDepartment of Ophthalmology, College of Medicine, National Cheng Kung University Hospital, National Cheng Kung University, Tainan, Taiwan.
Sung-Huei TsengDepartment of Ophthalmology, College of Medicine, National Cheng Kung University Hospital, National Cheng Kung University, Tainan, Taiwan.
Edward M ConwayCentre for Blood Research, University of British Columbia, Vancouver, BC, Canada.
Hua-Lin WuInternational Center for Wound Repair and Regeneration, National Cheng Kung University, Tainan, Taiwan. halnwu@mail.ncku.edu.tw.
National Cheng Kung University Hospital · TWNational Cheng Kung University · TWUniversity of British Columbia · CA

Funding

Ministry of Science and Technology, Taiwan 109-2628-B-006-032Ministry of Science and Technology, Taiwan 110-2320-B-006-051
6 · The paper itself

Abstract

Pathological angiogenesis (PA) contributes to various ocular diseases, including age-related macular degeneration, diabetic retinopathy, and retinopathy of prematurity, which are major causes of blindness over the world. Current treatments focus on anti-vascular endothelial growth factor (VEGF) therapy, but persistent avascular retina, recurrent intravitreal neovascularization, and general adverse effects are reported. We have previously found that recombinant thrombomodulin domain 1 (rTMD1) can suppress vascular inflammation. However, the function of rTMD1 in VEGF-induced PA remains unknown. In this study, we found that rTMD1 inhibited VEGF-induced angiogenesis in vitro. In an oxygen induced retinopathy (OIR) animal model, rTMD1 treatment significantly decreased retinal neovascularization but spared normal physiological vessel growth. Furthermore, loss of TMD1 significantly promoted PA in OIR. Meanwhile, hypoxia-inducible factor-1α, the transcription factor that upregulates VEGF, was suppressed after rTMD1 treatment. The levels of interleukin-6, and intercellular adhesion molecule-1 were also significantly suppressed. In conclusion, our results indicate that rTMD1 not only has dual effects to suppress PA and inflammation in OIR, but also can be a potential HIF-1α inhibitor for clinical use. These data bring forth the possibility of rTMD1 as a novel therapeutic agent for PA.

Indexed as

Gene Expression RegulationAnimalsApoptosisCell MovementCell ProliferationCells, CulturedFemaleHumansHypoxia-Inducible Factor 1, alpha SubunitMaleMiceMice, Inbred C57BLMice, KnockoutNeovascularization, PathologicRetinal NeovascularizationThrombomodulinHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitTHBD protein, humanThrombomodulinVascular Endothelial Growth Factor AVEGFA protein, humanHypoxia-inducible factor-1α (HIF-1α)Oxygen induced retinopathy (OIR)Pathological angiogenesis (PA)Recombinant thrombomodulin domain 1 (rTMD1)Vascular endothelial growth factor (VEGF)

Identifiers

PMID34705054
PMCPMC11072095
OpenAlexW3209921245

What OpenQuestion holds

Textmetadata
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.