Evidence map›Paper›PMID 30760202›Full record

ArticleMolecular medicine (Cambridge, Mass.)2019

Angiopoietin 1 influences ischemic reperfusion renal injury via modulating endothelium survival and regeneration.

Wen-Chih Chiang, Yu-Chin Huang, Ten-I Fu, Ping-Min Chen, Fan-Chi Chang, Chun-Fu Lai, Vin-Cent Wu, Shuei-Liong Lin, Yung-Ming Chen

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Review
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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

9 authors at 3 institutions in 1 country.

Wen-Chih ChiangDepartment of Internal Medicine, National Taiwan University Hospital, No. 7, Jhong-Shan South Road, Taipei, 100, Taiwan.
Yu-Chin HuangDepartment of Internal Medicine, Taoyuan General Hospital, Ministry of Health and Welfare, Taoyuan City, Taiwan.
Ten-I FuDepartment of Internal Medicine, National Taiwan University Hospital, No. 7, Jhong-Shan South Road, Taipei, 100, Taiwan.
Ping-Min ChenDepartment of Internal Medicine, National Taiwan University Hospital, No. 7, Jhong-Shan South Road, Taipei, 100, Taiwan.
Fan-Chi ChangDepartment of Internal Medicine, National Taiwan University Hospital, No. 7, Jhong-Shan South Road, Taipei, 100, Taiwan.
Chun-Fu LaiDepartment of Internal Medicine, National Taiwan University Hospital, No. 7, Jhong-Shan South Road, Taipei, 100, Taiwan.
Vin-Cent WuDepartment of Internal Medicine, National Taiwan University Hospital, No. 7, Jhong-Shan South Road, Taipei, 100, Taiwan.
Shuei-Liong LinDepartment of Internal Medicine, National Taiwan University Hospital, No. 7, Jhong-Shan South Road, Taipei, 100, Taiwan.
Yung-Ming ChenDepartment of Internal Medicine, National Taiwan University Hospital, No. 7, Jhong-Shan South Road, Taipei, 100, Taiwan. chenym@ntuh.gov.tw.
National Taiwan University Hospital · TWNational Yang Ming Chiao Tung University · TWTao Yuan General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDamage to the endothelium due to ischemia reperfusion injury (IRI) leads to a disruption of the microvasculature, which could be influenced by angiopoietin 1 via its effects on endothelium. We investigated the physiological and therapeutic roles of angiopoietin 1 in renal IRI using angiopoietin 1 knockout and over-expression mice.

methodsRenal IRI was induced by clamping the right renal artery seven days after left uninephrectomy for 25 min followed by reperfusion. A whole body angiopoietin 1 knockout was achieved by induction with tamoxifen. The renal tubule over-expression of angiopoietin 1 was induced by doxycycline.

resultsIn the normal mice, the renal expression of angiopoietin 1 increased 7 days to 14 days after IRI. The angiopoietin 1 knockout caused a delay in the recovery of renal function, less tubular regeneration and more residual tubular necrosis. The endothelial density was lower and the VE-cadherin protein loss was greater in the knockout mice. The over-expression of angiopoietin 1 attenuated the tubular necrosis and renal function impairment 1 and 3 days after IRI. The loss of the endothelium was ameliorated in the over-expression mice. This protective effect was associated with the up-regulation of the gene expression of epidermal growth factor, hepatocyte growth factor, and insulin like growth factor-1 and less tubular apoptosis. The over-expression of angiopoietin 1 stimulated tumor necrosis factor-α, C-C chemokine receptor type 2 and CX3C chemokine receptor 1 inflammatory gene expression, but did not influence macrophage infiltration.

conclusionsAltogether, the augmentation and downregulation of angiopoietin 1 attenuated renal damage and impaired renal recovery, respectively, by influencing the survival/regeneration of the endothelium. The manipulation of angiopoietin 1 represents a novel therapeutic approach for the treatment of ischemic kidney injury.

Indexed as

Acute Kidney InjuryAngiopoietin-1AnimalsDown-RegulationEndotheliumKidney TubulesMice, Inbred C57BLMice, TransgenicRegenerationReperfusion InjuryAngiopoietin-1Angpt1 protein, mouseAcute kidney injuryAngiopoietin 1EndotheliumIschemic reperfusion injuryKidney

Identifiers

PMID30760202
PMCPMC6375134
OpenAlexW2924236814

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.