Evidence map›Paper›PMID 28970293›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2017

Mitochondrial Respiration Is Reduced in Atherosclerosis, Promoting Necrotic Core Formation and Reducing Relative Fibrous Cap Thickness.

Emma P K Yu, Johannes Reinhold, Haixiang Yu, Lakshi Starks, Anna K Uryga, Kirsty Foote, Alison Finigan, Nichola Figg, Yuh-Fen Pung, Angela Logan and 2 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 119 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed, 1 pooled it
5.8field-weighted citation impact, top 3% 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

119 citing papers in PubMed, 1 synthesis or guideline pooled it, 160 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Myeloid Cell-Specific Deletion of LGR4 Suppresses Atherosclerotic Lesion Formation.Arteriosclerosis, thrombosis, and vascular biology · 2026
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  15. Xcr1eLife · 2025
    Article
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  19. Article
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59 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 1 institution in 1 country.

Emma P K YuFrom the Division of Cardiovascular Medicine, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, University of Cambridge, United Kingdom (E.P.K.Y., J.R., H.Y., L.S., A.K.U., K.F., A.F., N.F., M.B.); Department of Biomedical Sciences, University of Nottingham, Malaysia Campus, Selangor, Malaysia (Y.-F.P.); and MRC Mitochondrial Biology Unit, Cambridge, United Kingdom (A.L., M.P.M.). epky2@cam.ac.uk mrb@mole.bio.cam.ac.uk.
Johannes ReinholdFrom the Division of Cardiovascular Medicine, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, University of Cambridge, United Kingdom (E.P.K.Y., J.R., H.Y., L.S., A.K.U., K.F., A.F., N.F., M.B.); Department of Biomedical Sciences, University of Nottingham, Malaysia Campus, Selangor, Malaysia (Y.-F.P.); and MRC Mitochondrial Biology Unit, Cambridge, United Kingdom (A.L., M.P.M.).
Haixiang YuFrom the Division of Cardiovascular Medicine, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, University of Cambridge, United Kingdom (E.P.K.Y., J.R., H.Y., L.S., A.K.U., K.F., A.F., N.F., M.B.); Department of Biomedical Sciences, University of Nottingham, Malaysia Campus, Selangor, Malaysia (Y.-F.P.); and MRC Mitochondrial Biology Unit, Cambridge, United Kingdom (A.L., M.P.M.).
Lakshi StarksFrom the Division of Cardiovascular Medicine, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, University of Cambridge, United Kingdom (E.P.K.Y., J.R., H.Y., L.S., A.K.U., K.F., A.F., N.F., M.B.); Department of Biomedical Sciences, University of Nottingham, Malaysia Campus, Selangor, Malaysia (Y.-F.P.); and MRC Mitochondrial Biology Unit, Cambridge, United Kingdom (A.L., M.P.M.).
Anna K UrygaFrom the Division of Cardiovascular Medicine, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, University of Cambridge, United Kingdom (E.P.K.Y., J.R., H.Y., L.S., A.K.U., K.F., A.F., N.F., M.B.); Department of Biomedical Sciences, University of Nottingham, Malaysia Campus, Selangor, Malaysia (Y.-F.P.); and MRC Mitochondrial Biology Unit, Cambridge, United Kingdom (A.L., M.P.M.).
Kirsty FooteFrom the Division of Cardiovascular Medicine, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, University of Cambridge, United Kingdom (E.P.K.Y., J.R., H.Y., L.S., A.K.U., K.F., A.F., N.F., M.B.); Department of Biomedical Sciences, University of Nottingham, Malaysia Campus, Selangor, Malaysia (Y.-F.P.); and MRC Mitochondrial Biology Unit, Cambridge, United Kingdom (A.L., M.P.M.).
Alison FiniganFrom the Division of Cardiovascular Medicine, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, University of Cambridge, United Kingdom (E.P.K.Y., J.R., H.Y., L.S., A.K.U., K.F., A.F., N.F., M.B.); Department of Biomedical Sciences, University of Nottingham, Malaysia Campus, Selangor, Malaysia (Y.-F.P.); and MRC Mitochondrial Biology Unit, Cambridge, United Kingdom (A.L., M.P.M.).
Nichola FiggFrom the Division of Cardiovascular Medicine, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, University of Cambridge, United Kingdom (E.P.K.Y., J.R., H.Y., L.S., A.K.U., K.F., A.F., N.F., M.B.); Department of Biomedical Sciences, University of Nottingham, Malaysia Campus, Selangor, Malaysia (Y.-F.P.); and MRC Mitochondrial Biology Unit, Cambridge, United Kingdom (A.L., M.P.M.).
Yuh-Fen PungFrom the Division of Cardiovascular Medicine, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, University of Cambridge, United Kingdom (E.P.K.Y., J.R., H.Y., L.S., A.K.U., K.F., A.F., N.F., M.B.); Department of Biomedical Sciences, University of Nottingham, Malaysia Campus, Selangor, Malaysia (Y.-F.P.); and MRC Mitochondrial Biology Unit, Cambridge, United Kingdom (A.L., M.P.M.).
Angela LoganFrom the Division of Cardiovascular Medicine, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, University of Cambridge, United Kingdom (E.P.K.Y., J.R., H.Y., L.S., A.K.U., K.F., A.F., N.F., M.B.); Department of Biomedical Sciences, University of Nottingham, Malaysia Campus, Selangor, Malaysia (Y.-F.P.); and MRC Mitochondrial Biology Unit, Cambridge, United Kingdom (A.L., M.P.M.).
Michael P MurphyFrom the Division of Cardiovascular Medicine, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, University of Cambridge, United Kingdom (E.P.K.Y., J.R., H.Y., L.S., A.K.U., K.F., A.F., N.F., M.B.); Department of Biomedical Sciences, University of Nottingham, Malaysia Campus, Selangor, Malaysia (Y.-F.P.); and MRC Mitochondrial Biology Unit, Cambridge, United Kingdom (A.L., M.P.M.).
Martin BennettFrom the Division of Cardiovascular Medicine, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, University of Cambridge, United Kingdom (E.P.K.Y., J.R., H.Y., L.S., A.K.U., K.F., A.F., N.F., M.B.); Department of Biomedical Sciences, University of Nottingham, Malaysia Campus, Selangor, Malaysia (Y.-F.P.); and MRC Mitochondrial Biology Unit, Cambridge, United Kingdom (A.L., M.P.M.). epky2@cam.ac.uk mrb@mole.bio.cam.ac.uk.
University of Nottingham Malaysia Campus · MY

Funding

British Heart Foundation CH/2000003/12800British Heart Foundation FS/10/70/28507British Heart Foundation PG/11/57/29003British Heart Foundation PG/13/25/30014British Heart Foundation PG/14/69/31032British Heart Foundation PG/16/11/32021British Heart Foundation PG/16/63/32307British Heart Foundation RG/13/14/30314Medical Research Council MC_U105663142Medical Research Council MC_UU_00015/3Wellcome Trust 110158/Z/15/ZWellcome Trust 110159/Z/15/Z
6 · The paper itself

Abstract

objectiveMitochondrial DNA (mtDNA) damage is present in murine and human atherosclerotic plaques. However, whether endogenous levels of mtDNA damage are sufficient to cause mitochondrial dysfunction and whether decreasing mtDNA damage and improving mitochondrial respiration affects plaque burden or composition are unclear. We examined mitochondrial respiration in human atherosclerotic plaques and whether augmenting mitochondrial respiration affects atherogenesis. APPROACH AND

resultsHuman atherosclerotic plaques showed marked mitochondrial dysfunction, manifested as reduced mtDNA copy number and oxygen consumption rate in fibrous cap and core regions. Vascular smooth muscle cells derived from plaques showed impaired mitochondrial respiration, reduced complex I expression, and increased mitophagy, which was induced by oxidized low-density lipoprotein. Apolipoprotein E-deficient (ApoE

conclusionsEndogenous mtDNA damage in mouse and human atherosclerosis is associated with significantly reduced mitochondrial respiration. Reducing mtDNA damage and increasing mitochondrial respiration decrease necrotic core and increase fibrous cap areas independently of changes in reactive oxygen species and may be a promising therapeutic strategy in atherosclerosis.

Indexed as

DNA DamagePlaque, AtheroscleroticAnimalsAtherosclerosisBone Marrow TransplantationCell RespirationDisease Models, AnimalDNA HelicasesDNA, MitochondrialFemaleFibrosisGenetic Predisposition to DiseaseHumansMacrophagesMaleMice, Inbred C57BLDNA HelicasesDNA, MitochondrialMitochondrial ProteinsReactive Oxygen SpeciesTWNK protein, humanTwnk protein, mouseatherosclerosismitochondriareactive oxygen speciesrespirationvascular smooth muscle

Identifiers

PMID28970293
PMCPMC5701734
OpenAlexW2758507511

What OpenQuestion holds

Textmetadata
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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.