Evidence map›Paper›PMID 26801307›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2016

Myocyte repolarization modulates myocardial function in aging dogs.

Andrea Sorrentino, Sergio Signore, Khaled Qanud, Giulia Borghetti, Marianna Meo, Antonio Cannata, Yu Zhou, Ewa Wybieralska, Marco Luciani, Ramaswamy Kannappan and 15 more

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Phosphorylation of cardiac sodium channel at Ser571 anticipates manifestations of the aging myopathy.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  5. American journal of physiology. Heart and circulatory physiology · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Stop the beat to see the rhythm: excitation-contraction uncoupling in cardiac research.American journal of physiology. Heart and circulatory physiology · 2021
    Review
  10. Article
  11. Rhythm dynamics of the aging heart: an experimental study using conscious, restrained mice.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  12. Article
  13. Notch signaling modulates the electrical behavior of cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2018
    Article
  14. Age-related impairment of metabovascular coupling during cortical spreading depolarizations.American journal of physiology. Heart and circulatory physiology · 2017
    Article
  15. Hyperglycemia induces defective Ca2+ homeostasis in cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2017
    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

25 authors at 4 institutions in 1 country.

Andrea SorrentinoDepartments of Anesthesia and Medicine, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Sergio SignoreDepartments of Anesthesia and Medicine, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Khaled QanudDepartment of Physiology, New York Medical College, Valhalla, New York;ORCID http://orcid.org/0000-0003-2943-1245
Giulia BorghettiDepartments of Anesthesia and Medicine, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Marianna MeoDepartments of Anesthesia and Medicine, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Antonio CannataDepartments of Anesthesia and Medicine, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Yu ZhouDepartments of Anesthesia and Medicine, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Ewa WybieralskaDepartments of Anesthesia and Medicine, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Marco LucianiDepartments of Anesthesia and Medicine, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Ramaswamy KannappanDepartments of Anesthesia and Medicine, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Eric ZhangDepartments of Anesthesia and Medicine, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Alex MatsudaDepartments of Anesthesia and Medicine, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Andrew WebsterDepartments of Anesthesia and Medicine, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Maria CiminiDepartments of Anesthesia and Medicine, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Elizabeth KertowidjojoDepartment of Physiology, New York Medical College, Valhalla, New York;
David A D'AlessandroDepartment of Physiology, New York Medical College, Valhalla, New York;
Oriyanhan WunimengheDepartment of Cardiovascular and Thoracic Surgery, Montefiore Medical Center, Albert Einstein College of Medicine, New York, New York; and.
Robert E MichlerDepartment of Cardiovascular and Thoracic Surgery, Montefiore Medical Center, Albert Einstein College of Medicine, New York, New York; and.
Christopher RoyerLovelace Respiratory Research Institute, Albuquerque, New Mexico.
Polina GoichbergDepartments of Anesthesia and Medicine, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Annarosa LeriDepartments of Anesthesia and Medicine, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Edward G BarrettLovelace Respiratory Research Institute, Albuquerque, New Mexico.
Piero AnversaDepartments of Anesthesia and Medicine, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts;
Thomas H HintzeDepartment of Physiology, New York Medical College, Valhalla, New York;
Marcello RotaDepartments of Anesthesia and Medicine, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; Department of Physiology, New York Medical College, Valhalla, New York; marcello_rota@nymc.edu.
Brigham and Women's Hospital · USNew York Medical College · USAlbert Einstein College of Medicine · USLovelace Respiratory Research Institute · US

Funding

Rebuilding the Failing HeartP01HL092868 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI ANVERSA, PIERO · 2008 to 2013
$12.9M
Repair and Angiogenesis by Stem Cells in Human HeartR37HL081737 · NHLBI · NEW YORK MEDICAL COLLEGE · PI ANVERSA, PIERO · 2005 to 2015
$6.5M
Stem Cells and Myocardial Aging in DogsP01AG043353 · NIA · UNIVERSITY OF ALBUQUERQUE · PI ANVERSA, PIERO · 2013 to 2015
$4.5M
Stem Cells in the Developing HeartR01HL091021 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI ROTA, MARCELLO · 2009 to 2013
$2.4M
Redefining Human Myocardial BiologyR01HL105532 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI ANVERSA, PIERO, BUCHHOLZ, BRUCE A · 2011 to 2014
$2.2M
Immortal DNA Strand and Cardiac Stem Cell AgingR01AG037495 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI ANVERSA, PIERO · 2011 to 2014
$2.0M
Telomeric Shortening, p53 and miR-34a Condition Senescence of Cardiac ProgenitorsR01AG037490 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI LERI, ANNAROSA · 2010 to 2014
$1.7M
Cardiomyogenesis in the Adult HeartR01HL114346 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LERI, ANNAROSA, ROTA, MARCELLO · 2012 to 2015
$1.7M
Cardiac Stem Cells and AngiomyogenesisR01HL111183 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LERI, ANNAROSA · 2012 to 2015
$1.7M
Ephrin A1/EphA2 Signaling and Myocardial AgingR01AG044455 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI GOIHBERG, POLINA · 2014 to 2014
$351k
NHLBI NIH HHS P01-HL-092868NHLBI NIH HHS R01-HL-091021NHLBI NIH HHS R01-HL-105532NHLBI NIH HHS R01-HL-111183NHLBI NIH HHS R01-HL-114346NHLBI NIH HHS R37-HL-081737NIA NIH HHS P01-AG-043353NIA NIH HHS R01-AG-037490NIA NIH HHS R01-AG-037495NIA NIH HHS R01-AG-044455
6 · The paper itself

Abstract

Studies of myocardial aging are complex and the mechanisms involved in the deterioration of ventricular performance and decreased functional reserve of the old heart remain to be properly defined. We have studied a colony of beagle dogs from 3 to 14 yr of age kept under a highly regulated environment to define the effects of aging on the myocardium. Ventricular, myocardial, and myocyte function, together with anatomical and structural properties of the organ and cardiomyocytes, were evaluated. Ventricular hypertrophy was not observed with aging and the structural composition of the myocardium was modestly affected. Alterations in the myocyte compartment were identified in aged dogs, and these factors negatively interfere with the contractile reserve typical of the young heart. The duration of the action potential is prolonged in old cardiomyocytes contributing to the slower electrical recovery of the myocardium. Also, the remodeled repolarization of cardiomyocytes with aging provides inotropic support to the senescent muscle but compromises its contractile reserve, rendering the old heart ineffective under conditions of high hemodynamic demand. The defects in the electrical and mechanical properties of cardiomyocytes with aging suggest that this cell population is an important determinant of the cardiac senescent phenotype. Collectively, the delayed electrical repolarization of aging cardiomyocytes may be viewed as a critical variable of the aging myopathy and its propensity to evolve into ventricular decompensation under stressful conditions.

Indexed as

Action PotentialsVentricular FunctionAgingAnimalsDogsFemaleHemodynamicsMaleMyocytes, Cardiacagingcontractile reservemyocardium

Identifiers

PMID26801307
PMCPMC4867360
OpenAlexW2289380269

What OpenQuestion holds

Textmetadata
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.