Evidence map›Paper›PMID 27941052›Full record

ReviewDiabetes & vascular disease research2017

Role of endoplasmic reticulum stress signalling in diabetic endothelial dysfunction and atherosclerosis.

Yunzhou Dong, Conrad Fernandes, Yanjun Liu, Yong Wu, Hao Wu, Megan L Brophy, Lin Deng, Kai Song, Aiyun Wen, Scott Wong and 3 more

Open access · bronzeAbstract readReview
In one paragraph

Review in Diabetes & vascular disease research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

56 citing papers in PubMed, 93 citations in OpenAlex.

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  9. Photodynamic Therapy for Atherosclerosis.International journal of molecular sciences · 2024
    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

13 authors at 6 institutions in 2 countries.

Yunzhou DongVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Conrad FernandesDepartment of Biosciences, Rice University, Houston, TX, USA.
Yanjun LiuDepartment of Internal Medicine, Charles R. Drew University of Medicine and Science, University of California-Los Angeles School of Medicine, Los Angeles, CA, USA.
Yong WuDepartment of Internal Medicine, Charles R. Drew University of Medicine and Science, University of California-Los Angeles School of Medicine, Los Angeles, CA, USA.
Hao WuVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Megan L BrophyVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Lin DengDepartment of Biological Chemistry & Molecular Pharmacology, Harvard Medical School, Boston, MA, USA.
Kai SongVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Aiyun WenVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Scott WongVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
Daoguang YanDepartment of Biology, Jinan University, Guangzhou, China.
Rheal TownerAdvanced Magnetic Resonance Center, Oklahoma Medical Research Foundation, Oklahoma, OK, USA.
Hong ChenVascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA hong.chen@childrens.harvard.edu.
Harvard University · USBoston Children's Hospital · USUniversity of California, Los Angeles · USJinan University · CNOklahoma Medical Research Foundation · USRice University · US

Funding

SWI/SNF-REGULATED POSTNATAL ANGIOGENESISP20RR018758 · NCRR · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI BARLIC-DICEN, JANA · 2003 to 2011
$14.9M
Epsin in Angiogenesis and Vascular RemodelingR01HL093242 · NHLBI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI CHEN, HONG, WANG, DA-ZHI · 2009 to 2021
$7.3M
Molecular Mechanisms Controlling Lymphatic Vascular Function in Health and DiseaseR01HL133216 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, HONG, DIXON, JAMES BRANDON · 2016 to 2025
$6.7M
Mechanisms regulating VEGF receptors in diabetic angiogenesisR01HL130845 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, HONG, XU, JIAN · 2016 to 2023
$4.9M
Molecular Mechanisms Regulating Endothelial DysfunctionR01HL137229 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI CHEN, HONG, SRIVASTAVA, SANJAY · 2017 to 2020
$2.7M
The Role of Signaling Adaptor Protein Epsin in AtherosclerosisR01HL118676 · NHLBI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI CHEN, HONG · 2014 to 2017
$1.8M
Mechanisms behind hyperglycemia-associated breast cancer risk and progressionSC1CA200517 · NCI · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI WU, YONG · 2015 to 2018
$1.4M
The Role of Adipose H6PDH in Type 2 Diabetes and ObesitySC1DK104821 · NIDDK · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI LIU, YANJUN · 2014 to 2017
$1.3M
Molecular Mechanisms Regulating Epsin-Dependent LRP-1 Internalization and Degradation in AtherosclerosisF31HL127982 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI BROPHY, MEGAN · 2015 to 2017
$101k
NCI NIH HHS SC1 CA200517NCRR NIH HHS P20 RR018758NHLBI NIH HHS F31 HL127982NHLBI NIH HHS R01 HL093242NHLBI NIH HHS R01 HL118676NHLBI NIH HHS R01 HL130845NHLBI NIH HHS R01 HL133216NHLBI NIH HHS R01 HL137229NIDDK NIH HHS SC1 DK104821
6 · The paper itself

Abstract

It is well established that diabetes mellitus accelerates atherosclerotic vascular disease. Endothelial injury has been proposed to be the initial event in the pathogenesis of atherosclerosis. Endothelium not only acts as a semi-selective barrier but also serves physiological and metabolic functions. Diabetes or high glucose in circulation triggers a series of intracellular responses and organ damage such as endothelial dysfunction and apoptosis. One such response is high glucose-induced chronic endoplasmic reticulum stress in the endothelium. The unfolded protein response is an acute reaction that enables cells to overcome endoplasmic reticulum stress. However, when chronically persistent, endoplasmic reticulum stress response could ultimately lead to endothelial dysfunction and atherosclerosis. Herein, we discuss the scientific advances in understanding endoplasmic reticulum stress-induced endothelial dysfunction, the pathogenesis of diabetes-accelerated atherosclerosis and endoplasmic reticulum stress as a potential target in therapies for diabetic atherosclerosis.

Indexed as

Endoplasmic Reticulum StressSignal TransductionAnimalsAtherosclerosisCardiovascular AgentsDiabetic AngiopathiesEndoplasmic ReticulumEndothelial CellsEndothelium, VascularHumansPlaque, AtheroscleroticCardiovascular AgentsatherosclerosisDiabetes mellitusendoplasmic reticulum stressendothelial dysfunction

Identifiers

PMID27941052
PMCPMC5161113
OpenAlexW2534946788

What OpenQuestion holds

Textmetadata
LicenceTDM
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.