Evidence map›Paper›PMID 34173824›Full record

ArticleCardiovascular research2022

Human coronary microvascular contractile dysfunction associates with viable synthetic smooth muscle cells.

Kim A Dora, Lyudmyla Borysova, Xi Ye, Chloe Powell, Timea Z Beleznai, Christopher P Stanley, Vito D Bruno, Tobias Starborg, Errin Johnson, Anna Pielach and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Cardiovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Intramyocardial immunomodulation with human CD16Frontiers in cardiovascular medicine · 2024
    Article
  7. Article
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  9. 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

13 authors at 4 institutions in 1 country.

Kim A DoraThe Vascular Pharmacology Group, Department of Pharmacology, University of Oxford, Mansfield Road, Oxford, OX1 3QT, UK.ORCID 0000-0002-8014-2775
Lyudmyla BorysovaThe Vascular Pharmacology Group, Department of Pharmacology, University of Oxford, Mansfield Road, Oxford, OX1 3QT, UK.ORCID 0000-0003-0458-9871
Xi YeThe Vascular Pharmacology Group, Department of Pharmacology, University of Oxford, Mansfield Road, Oxford, OX1 3QT, UK.ORCID 0000-0002-1694-2786
Chloe PowellThe Vascular Pharmacology Group, Department of Pharmacology, University of Oxford, Mansfield Road, Oxford, OX1 3QT, UK.ORCID 0000-0002-6816-1041
Timea Z BeleznaiThe Vascular Pharmacology Group, Department of Pharmacology, University of Oxford, Mansfield Road, Oxford, OX1 3QT, UK.
Christopher P StanleyThe Vascular Pharmacology Group, Department of Pharmacology, University of Oxford, Mansfield Road, Oxford, OX1 3QT, UK.
Vito D BrunoBristol Heart Institute and Translational Biomedical Research Centre, University of Bristol, Bristol Royal Infirmary, Upper Maudlin Street, Bristol, BS2 8HW, UK.ORCID 0000-0002-8193-9559
Tobias StarborgDivision of Cell Matrix Biology and Regenerative Medicine School of Biological Sciences Faculty of Biology, Medical and Health Sciences, University of Manchester, B.3016 Michael Smith Building, Oxford Road, Manchester, M13 9PT, UK.
Errin JohnsonSir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford, OX1 3RE, UK.
Anna PielachSir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford, OX1 3RE, UK.
Michael TaggartBiosciences Institute, Newcastle University, International Centre for Life, Central Parkway, Newcastle upon Tyne, NE1 3BZ, UK.ORCID 0000-0002-9981-2783
Nicola SmartDepartment of Physiology, Anatomy and Genetics, University of Oxford, Sherrington Building, Parks Road, Oxford, OX1 3PT, UK.ORCID 0000-0002-3501-7254
Raimondo AscioneBristol Heart Institute and Translational Biomedical Research Centre, University of Bristol, Bristol Royal Infirmary, Upper Maudlin Street, Bristol, BS2 8HW, UK.ORCID 0000-0001-8045-5619
University of Oxford · GBBristol Royal Infirmary · GBCentre for Life · GBUniversity of Manchester · GB

Funding

British Heart Foundation FS/08/033/25111British Heart Foundation FS/13/16/30199British Heart Foundation FS/13/4/30045British Heart Foundation IG/13/5/30431British Heart Foundation IG/14/2/30991British Heart Foundation PG/16/104/32652British Heart Foundation PG/18/11/33552British Heart Foundation PG/18/49/33833British Heart Foundation RE/13/1/30181Medical Research Council MR/L012723/1
6 · The paper itself

Abstract

aimsCoronary microvascular smooth muscle cells (SMCs) respond to luminal pressure by developing myogenic tone (MT), a process integral to the regulation of microvascular perfusion. The cellular mechanisms underlying poor myogenic reactivity in patients with heart valve disease are unknown and form the focus of this study. METHODS AND

resultsIntramyocardial coronary micro-arteries (IMCAs) isolated from human and pig right atrial (RA) appendage and left ventricular (LV) biopsies were studied using pressure myography combined with confocal microscopy. All RA- and LV-IMCAs from organ donors and pigs developed circa 25% MT. In contrast, 44% of human RA-IMCAs from 88 patients with heart valve disease had poor (<10%) MT yet retained cell viability and an ability to raise cytoplasmic Ca2+ in response to vasoconstrictor agents. Comparing across human heart chambers and species, we found that based on patient medical history and six tests, the strongest predictor of poor MT in IMCAs was increased expression of the synthetic marker caldesmon relative to the contractile marker SM-myosin heavy chain. In addition, high resolution imaging revealed a distinct layer of longitudinally aligned SMCs between ECs and radial SMCs, and we show poor MT was associated with disruptions in these cellular alignments.

conclusionThese data demonstrate the first use of atrial and ventricular biopsies from patients and pigs to reveal that impaired coronary MT reflects a switch of viable SMCs towards a synthetic phenotype, rather than a loss of SMC viability. These arteries represent a model for further studies of coronary microvascular contractile dysfunction.

Indexed as

Heart Valve DiseasesMuscle, Smooth, VascularAnimalsCoronary VesselsHumansMuscle ContractionMyocytes, Smooth MuscleSwineCa2+Coronary arteriolesCoronary microvascular functionHeart valve diseaseHumanMicrovascular perfusionMyogenic tonesignallingSmooth muscle cellSynthetic phenotypeUltrastructure

Identifiers

PMID34173824
PMCPMC9239576
OpenAlexW3176614485

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.