Evidence map›Paper›PMID 26780888›Full record

ArticleAging cell2016

Intact endothelial autophagy is required to maintain vascular lipid homeostasis.

Kumiko Torisu, Krishna K Singh, Takehiro Torisu, Fina Lovren, Jie Liu, Yi Pan, Adrian Quan, Azza Ramadan, Mohammed Al-Omran, Natalie Pankova and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
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 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

81 citing papers in PubMed, 127 citations in OpenAlex.

  1. Review
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  5. Decoding Vascular Senescence: Cellular Insights and Therapeutic Strategies.International journal of biological sciences · 2026
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21 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Kumiko TorisuCenter for Molecular Medicine, National Heart, Lung and Blood Institute, NIH, 10 Center Drive, Bethesda, MD 20892, USA.
Krishna K SinghDivision of Cardiac Surgery, Keenan Research Centre for Biomedical Sciences, St. Michael's Hospital, University of Toronto, 30 Bond Street, Toronto, ON M5B 1W8, Canada.
Takehiro TorisuCenter for Molecular Medicine, National Heart, Lung and Blood Institute, NIH, 10 Center Drive, Bethesda, MD 20892, USA.
Fina LovrenDivision of Cardiac Surgery, Keenan Research Centre for Biomedical Sciences, St. Michael's Hospital, University of Toronto, 30 Bond Street, Toronto, ON M5B 1W8, Canada.
Jie LiuCenter for Molecular Medicine, National Heart, Lung and Blood Institute, NIH, 10 Center Drive, Bethesda, MD 20892, USA.
Yi PanDivision of Cardiac Surgery, Keenan Research Centre for Biomedical Sciences, St. Michael's Hospital, University of Toronto, 30 Bond Street, Toronto, ON M5B 1W8, Canada.
Adrian QuanDivision of Cardiac Surgery, Keenan Research Centre for Biomedical Sciences, St. Michael's Hospital, University of Toronto, 30 Bond Street, Toronto, ON M5B 1W8, Canada.
Azza RamadanDivision of Cardiac Surgery, Keenan Research Centre for Biomedical Sciences, St. Michael's Hospital, University of Toronto, 30 Bond Street, Toronto, ON M5B 1W8, Canada.
Mohammed Al-OmranDivision of Vascular Surgery, Keenan Research Centre for Biomedical Sciences, St. Michael's Hospital, University of Toronto, 30 Bond Street, Toronto, ON M5B 1W8, Canada.
Natalie PankovaDepartment of Ophthalmology and Vision Sciences, Keenan Research Centre for Biomedical Sciences, St. Michael's Hospital, University of Toronto, 30 Bond Street, Toronto, ON M5B 1W8, Canada.
Shelley R BoydDepartment of Ophthalmology and Vision Sciences, Keenan Research Centre for Biomedical Sciences, St. Michael's Hospital, University of Toronto, 30 Bond Street, Toronto, ON M5B 1W8, Canada.
Subodh VermaDivision of Cardiac Surgery, Keenan Research Centre for Biomedical Sciences, St. Michael's Hospital, University of Toronto, 30 Bond Street, Toronto, ON M5B 1W8, Canada.
Toren FinkelCenter for Molecular Medicine, National Heart, Lung and Blood Institute, NIH, 10 Center Drive, Bethesda, MD 20892, USA.
St. Michael's Hospital · CANational Heart Lung and Blood Institute · USUniversity of Toronto · CA

Funding

NHLBI Animal Program DivisionZIGHL006020 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI CLARK, TANNIA · 2009 to 2025
$47.3M
The role of autophagy in aging and metabolismZIAHL005012 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI FINKEL, TOREN · 2009 to 2017
$11.8M
Canadian Institutes of Health ResearchIntramural NIH HHS
6 · The paper itself

Abstract

The physiological role of autophagic flux within the vascular endothelial layer remains poorly understood. Here, we show that in primary endothelial cells, oxidized and native LDL stimulates autophagosome formation. Moreover, by both confocal and electron microscopy, excess native or modified LDL appears to be engulfed within autophagic structures. Transient knockdown of the essential autophagy gene ATG7 resulted in higher levels of intracellular (125) I-LDL and oxidized LDL (OxLDL) accumulation, suggesting that in endothelial cells, autophagy may represent an important mechanism to regulate excess, exogenous lipids. The physiological importance of these observations was assessed using mice containing a conditional deletion of ATG7 within the endothelium. Following acute intravenous infusion of fluorescently labeled OxLDL, mice lacking endothelial expression of ATG7 demonstrated prolonged retention of OxLDL within the retinal pigment epithelium (RPE) and choroidal endothelium of the eye. In a chronic model of lipid excess, we analyzed atherosclerotic burden in ApoE(-/-) mice with or without endothelial autophagic flux. The absence of endothelial autophagy markedly increased atherosclerotic burden. Thus, in both an acute and chronic in vivo model, endothelial autophagy appears critically important in limiting lipid accumulation within the vessel wall. As such, strategies that stimulate autophagy, or prevent the age-dependent decline in autophagic flux, might be particularly beneficial in treating atherosclerotic vascular disease.

Indexed as

AnimalsApolipoproteins EAtherosclerosisAutophagyCells, CulturedEndothelial CellsEndothelium, VascularHomeostasisLipid MetabolismLipoproteins, LDLMice, KnockoutOxidation-ReductionRetinal Pigment EpitheliumApolipoproteins ELipoproteins, LDLoxidized low density lipoproteinatherosclerosisautophagylipidsmouse

Identifiers

PMID26780888
PMCPMC4717267
OpenAlexW2179361784

What Socratic 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 Socratic graph.