Evidence map›Paper›PMID 28194400›Full record

ReviewFrontiers in cardiovascular medicine2017

Eating the Dead to Keep Atherosclerosis at Bay.

Megan L Brophy, Yunzhou Dong, Hao Wu, H N Ashiqur Rahman, Kai Song, Hong Chen

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

31 citing papers in PubMed, 73 citations in OpenAlex.

  1. Key parameters for designing robust 2D and 3D spheroid models forBioengineering & translational medicine · 2025
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  12. Pharmacologic modulation of intracellular NaProceedings of the National Academy of Sciences of the United States of America · 2022
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  15. Journal of clinical medicine · 2022
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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

6 authors at 3 institutions in 1 country.

Megan L BrophyDepartment of Biochemistry and Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA; Karp Family Research Laboratories, Vascular Biology Program, Harvard Medical School, Boston Children's Hospital, Boston, MA, USA.
Yunzhou DongKarp Family Research Laboratories, Vascular Biology Program, Harvard Medical School, Boston Children's Hospital , Boston, MA , USA.
Hao WuKarp Family Research Laboratories, Vascular Biology Program, Harvard Medical School, Boston Children's Hospital , Boston, MA , USA.
H N Ashiqur RahmanKarp Family Research Laboratories, Vascular Biology Program, Harvard Medical School, Boston Children's Hospital , Boston, MA , USA.
Kai SongKarp Family Research Laboratories, Vascular Biology Program, Harvard Medical School, Boston Children's Hospital , Boston, MA , USA.
Hong ChenKarp Family Research Laboratories, Vascular Biology Program, Harvard Medical School, Boston Children's Hospital , Boston, MA , USA.
Family Research Institute · USBoston Children's Hospital · USHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is the primary cause of coronary heart disease (CHD), ischemic stroke, and peripheral arterial disease. Despite effective lipid-lowering therapies and prevention programs, atherosclerosis is still the leading cause of mortality in the United States. Moreover, the prevalence of CHD in developing countries worldwide is rapidly increasing at a rate expected to overtake those of cancer and diabetes. Prominent risk factors include the hardening of arteries and high levels of cholesterol, which lead to the initiation and progression of atherosclerosis. However, cell death and efferocytosis are critical components of both atherosclerotic plaque progression and regression, yet, few currently available therapies focus on these processes. Thus, understanding the causes of cell death within the atherosclerotic plaque, the consequences of cell death, and the mechanisms of apoptotic cell clearance may enable the development of new therapies to treat cardiovascular disease. Here, we review how endoplasmic reticulum stress and cholesterol metabolism lead to cell death and inflammation, how dying cells affect plaque progression, and how autophagy and the clearance of dead cells ameliorates the inflammatory environment of the plaque. In addition, we review current research aimed at alleviating these processes and specifically targeting therapeutics to the site of the plaque.

Indexed as

apoptosisatherosclerosisautophagyefferocytosismacrophages

Identifiers

PMID28194400
PMCPMC5277199
OpenAlexW2580081338

What OpenQuestion 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 OpenQuestion graph.