Evidence map›Paper›PMID 27133203›Full record

ArticleAging cell2016

Deregulation of XBP1 expression contributes to myocardial vascular endothelial growth factor-A expression and angiogenesis during cardiac hypertrophy in vivo.

Quanlu Duan, Li Ni, Peihua Wang, Chen Chen, Lei Yang, Ben Ma, Wei Gong, Zhejun Cai, Ming-Hui Zou, Dao Wen Wang

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.0field-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

39 citing papers in PubMed, 68 citations in OpenAlex.

  1. Observational
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  12. Molecular Mechanism Underlying Role of the XBP1s in Cardiovascular Diseases.Journal of cardiovascular development and disease · 2022
    Review
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  18. Xbp1s-Ddit3 promotes MCT-induced pulmonary hypertension.Clinical science (London, England : 1979) · 2021
    Article
  19. Article
  20. Article
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

10 authors at 3 institutions in 2 countries.

Quanlu DuanDivision of Cardiology, Department Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People's Republic of China.
Li NiDivision of Cardiology, Department Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People's Republic of China.
Peihua WangDivision of Cardiology, Department Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People's Republic of China.
Chen ChenDivision of Cardiology, Department Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People's Republic of China.
Lei YangDivision of Cardiology, Department Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People's Republic of China.
Ben MaDivision of Cardiology, Department Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People's Republic of China.
Wei GongDivision of Cardiology, Department Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People's Republic of China.
Zhejun CaiDivision of Cardiology, Department Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People's Republic of China.
Ming-Hui ZouCenter for Molecular and Translational Medicine, Georgia State University, Atlanta, 30303, GA, USA.
Dao Wen WangDivision of Cardiology, Department Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People's Republic of China.
Huazhong University of Science and Technology · CNTongji Hospital · CNGeorgia State University · US

Funding

Reactive Nitrogen species and Diabetic Endothelial DysfunctionR01HL079584 · NHLBI · UNIVERSITY OF TENNESSEE KNOXVILLE · PI ZOU, MING-HUI · 2004 to 2021
$7.3M
Inflammasome and unstable atherosclerotic plaquesR01HL089920 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2008 to 2022
$6.9M
AMP-Activated Protein Kinase in DiabetesR01HL080499 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2006 to 2019
$5.8M
Controlling VSMC Proliferation and MigrationR01HL110488 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2011 to 2020
$3.9M
Oxidant stress and diabetic endothelial dysfunctionR01HL074399 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2005 to 2013
$3.2M
Suppression of Autophagy-Dependent Clearance Mitochondria in Type 2 DiabetesR01HL128014 · NHLBI · GEORGIA STATE UNIVERSITY · PI XIE, ZHONGLIN, ZOU, MING-HUI · 2015 to 2018
$2.4M
Prevention of High Fat Diet-Induced Vascular InjuryR01HL105157 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2010 to 2014
$1.8M
Angiotensin-II, GTPCH1 and 26S ProtesomesR01HL096032 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2009 to 2013
$1.8M
Sirt1, Vascular Aging, and Aortic AneurysmR01AG047776 · NIA · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2014 to 2018
$1.5M
NHLBI NIH HHS R01 HL074399NHLBI NIH HHS R01 HL079584NHLBI NIH HHS R01 HL080499NHLBI NIH HHS R01 HL089920NHLBI NIH HHS R01 HL096032NHLBI NIH HHS R01 HL105157NHLBI NIH HHS R01 HL110488NHLBI NIH HHS R01 HL128014NIA NIH HHS R01 AG047776
6 · The paper itself

Abstract

Endoplasmic reticulum (ER) stress has been reported to be involved in many cardiovascular diseases such as atherosclerosis, diabetes, myocardial ischemia, and hypertension that ultimately result in heart failure. XBP1 is a key ER stress signal transducer and an important pro-survival factor of the unfolded protein response (UPR) in mammalian cells. The aim of this study was to establish a role for XBP1 in the deregulation of pro-angiogenic factor VEGF expression and potential regulatory mechanisms in hypertrophic and failing heart. Western blots showed that myocardial XBP1s protein was significantly increased in both isoproterenol (ISO)-induced and pressure-overload-induced hypertrophic and failing heart compared to normal control. Furthermore, XBP1 silencing exacerbates ISO-induced cardiac dysfunction along with a reduction of myocardial capillary density and cardiac expression of pro-angiogenic factor VEGF-A in vivo. Consistently, experiments in cultured cardiomyocytes H9c2 (2-1) cells showed that UPR-induced VEGF-A upregulation was determined by XBP1 expression level. Importantly, VEGF-A expression was increased in failing human heart tissue and blood samples and was correlated with the levels of XBP1. These results suggest that XBP1 regulates VEGF-mediated cardiac angiogenesis, which contributes to the progression of adaptive hypertrophy, and might provide novel targets for prevention and treatment of heart failure.

Indexed as

AgedAnimalsCapillariesCardiomegalyCell LineDependovirusEndoplasmic Reticulum StressFemaleGene SilencingHeart FailureHumansIsoproterenolMaleMice, Inbred C57BLMiddle AgedModels, BiologicalIsoproterenolRNA, Small InterferingVascular Endothelial Growth Factor AX-Box Binding Protein 1XBP1 protein, humanXbp1 protein, mouseXbp1 protein, ratangiogenesiscardiac hypertrophyunfolded protein responsevascular endothelial growth factor-AXBP1

Identifiers

PMID27133203
PMCPMC4933664
OpenAlexW2345147999

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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.