Evidence map›Paper›PMID 27062403›Full record

ArticleAtherosclerosis2016

Biphasic alterations in coronary smooth muscle Ca(2+) regulation in a repeat cross-sectional study of coronary artery disease severity in metabolic syndrome.

Mikaela L McKenney-Drake, Stacey D Rodenbeck, Meredith K Owen, Kyle A Schultz, Mouhamad Alloosh, Johnathan D Tune, Michael Sturek

Open access · greenAbstract read
In one paragraph

Article in Atherosclerosis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.6field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Intracellular CaJournal of cardiovascular translational research · 2022
    Article
  3. Atherosclerosis Imaging withDiagnostics (Basel, Switzerland) · 2020
    Review
  4. Article
  5. Article
  6. Effect of metabolic syndrome and aging on CaExperimental gerontology · 2018
    Article
  7. Article
  8. Article
  9. Article
  10. 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

7 authors at 2 institutions in 1 country.

Mikaela L McKenney-DrakeDepartment of Cellular & Integrative Physiology, Indiana University School of Medicine, 635 Barnhill Dr., Indianapolis, IN 46202, USA; College of Pharmacy & Health Sciences, Butler University, 4600 Sunset Ave., Indianapolis, IN 46208, USA.
Stacey D RodenbeckDepartment of Cellular & Integrative Physiology, Indiana University School of Medicine, 635 Barnhill Dr., Indianapolis, IN 46202, USA.
Meredith K OwenDepartment of Cellular & Integrative Physiology, Indiana University School of Medicine, 635 Barnhill Dr., Indianapolis, IN 46202, USA; Covance, Inc., 671 South Meridian Road, Greenfield, IN 46140, USA.
Kyle A SchultzDepartment of Cellular & Integrative Physiology, Indiana University School of Medicine, 635 Barnhill Dr., Indianapolis, IN 46202, USA.
Mouhamad AllooshDepartment of Cellular & Integrative Physiology, Indiana University School of Medicine, 635 Barnhill Dr., Indianapolis, IN 46202, USA.
Johnathan D TuneDepartment of Cellular & Integrative Physiology, Indiana University School of Medicine, 635 Barnhill Dr., Indianapolis, IN 46202, USA.
Michael SturekDepartment of Cellular & Integrative Physiology, Indiana University School of Medicine, 635 Barnhill Dr., Indianapolis, IN 46202, USA. Electronic address: msturek@iu.edu.
Indiana University School of MedicineButler University · US

Funding

Indiana Clinical and Translational Sciences InstituteUL1TR001108 · NCATS · INDIANA UNIVERSITY INDIANAPOLIS · PI DENNE, SCOTT C., SHEKHAR, ANANTHA · 2013 to 2017
$23.3M
Translation CoreP30DK097512 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI Carmella Evans-Molina · 2015 to 2026
$17.4M
RESEARCH TRAINING PROGRAM IN DIABETES AND OBESITYT32DK064466 · NIDDK · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI Carmella Evans-Molina, RONALD C WEK · 2003 to 2026
$5.2M
EXERCISE, DIABETES, &CORONARY SMOOTH MUSCLE Ca2+R01HL062552 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI STUREK, MICHAEL · 1999 to 2013
$4.5M
Indiana Clinical and Translational Science Institute-T32 Program TL1TL1TR000162 · NCATS · INDIANA UNIVERSITY INDIANAPOLIS · PI SHEKHAR, ANANTHA · 2012 to 2013
$264k
NCATS NIH HHS TL1 TR000162NCATS NIH HHS UL1 TR001108NHLBI NIH HHS R01 HL062552NIDDK NIH HHS P30 DK097512NIDDK NIH HHS T32 DK064466
6 · The paper itself

Abstract

BACKGROUND AND

aimsCoronary artery disease (CAD) is progressive, classified by stages of severity. Alterations in Ca(2+) regulation within coronary smooth muscle (CSM) cells in metabolic syndrome (MetS) have been observed, but there is a lack of data in relatively early (mild) and late (severe) stages of CAD. The current study examined alterations in CSM Ca(2+) regulation at several time points during CAD progression.

methodsMetS was induced by feeding an excess calorie atherogenic diet for 6, 9, or 12 months and compared to age-matched lean controls. CAD was measured with intravascular ultrasound (IVUS). Intracellular Ca(2+) was assessed with fura-2.

resultsIVUS revealed that the extent of atherosclerotic CAD correlated with the duration on atherogenic diet. Fura-2 imaging of intracellular Ca(2+) in CSM cells revealed heightened Ca(2+) signaling at 9 months on diet, compared to 6 and 12 months, and to age-matched lean controls. Isolated coronary artery rings from swine fed for 9 months followed the same pattern, developing greater tension to depolarization, compared to 6 and 12 months (6 months = 1.8 ± 0.6 g, 9 months = 5.0 ± 1.0 g, 12 months = 0.7 ± 0.1 g). CSM in severe atherosclerotic plaques showed dampened Ca(2+) regulation and decreased proliferation compared to CSM from the wall.

conclusionsThese CSM Ca(2+) regulation data from several time points in CAD progression and severity help to resolve the controversy regarding up-vs. down-regulation of CSM Ca(2+) regulation in previous reports. These data are consistent with the hypothesis that alterations in sarcoplasmic reticulum Ca(2+) contribute to progression of atherosclerotic CAD in MetS.

Indexed as

AnimalsArteriesAtherosclerosisCalciumCalcium ChannelsCell ProliferationCoronary Artery DiseaseCross-Sectional StudiesDisease Models, AnimalDisease ProgressionMetabolic SyndromeMyocytes, Smooth MusclePhenotypeSarcoplasmic Reticulum Calcium-Transporting ATPasesSwineSwine, MiniatureCalciumCalcium ChannelsSarcoplasmic Reticulum Calcium-Transporting ATPasesCalcium regulationOssabaw swineProliferationSmooth muscle phenotype

Identifiers

PMID27062403
PMCPMC4879093
OpenAlexW2311083469

What OpenQuestion holds

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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.