Evidence map›Paper›PMID 20658186›Full record

ReviewHeart failure reviews2010

Modulation of beta-adrenergic receptor signaling in heart failure and longevity: targeting adenylyl cyclase type 5.

David Ho, Lin Yan, Kousaku Iwatsubo, Dorothy E Vatner, Stephen F Vatner

Abstract readReview
In one paragraph

Review in Heart failure reviews, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

43 citing papers in PubMed, 66 citations in OpenAlex.

  1. Drug Repositioning in Doxorubicin-Induced Cardiotoxicity Protection.International journal of molecular sciences · 2025
    Review
  2. Article
  3. AI approaches for the discovery and validation of drug targets.Cambridge prisms. Precision medicine · 2024
    Review
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  17. βAnimal cells and systems · 2019
    Article
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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

5 authors at 2 institutions in 1 country.

David HoDepartment of Cell Biology and Molecular Medicine and The Cardiovascular Research Institute, University of Medicine & Dentistry of New Jersey, New Jersey Medical School, 185 South Orange Avenue, MSB G609, Newark, NJ 07103, USA.
Lin Yan
Kousaku Iwatsubo
Dorothy E Vatner
Stephen F Vatner
Rutgers New Jersey Medical SchoolRutgers, The State University of New Jersey · US

Funding

Molecular Mechanisms in Chronically Stunned MyocardiumP01HL069020 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI VATNER, DOROTHY EILEEN · 2001 to 2014
$21.3M
SARCOMERIC PROTEIN MUTATIONS IN HYPERTROPHY AND HEART FAILUREP01HL059139 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI RYDEN, EVA B · 1997 to 2007
$12.4M
Longevity and Stress ResistanceP01AG027211 · NIA · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI VATNER, STEPHEN F · 2007 to 2013
$10.3M
CARDIOVASCULAR CONTROL IN NORMAL AND DISEASE STATESR01HL033107 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI VATNER, STEPHEN F · 1985 to 2011
$6.2M
AGING EFFECTS ON CARDIOVASCULAR FUNCTION IN PRIMATESR01AG014121 · NIA · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI VATNER, STEPHEN F · 1996 to 2007
$3.5M
Integrative Mechanisms in Cardiovascular DiseaseT32HL069752 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI VATNER, STEPHEN F · 2004 to 2013
$2.9M
Intrinsic Vascular Smooth Muscle Cell StiffnessR01HL102472 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI VATNER, STEPHEN F · 2010 to 2016
$2.5M
Adenylyl cyclase isoforms in hypertrophy and heart failureR01HL093481 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI VATNER, STEPHEN F · 2009 to 2013
$2.3M
Rescue of Beta-Adrenergic Cardiomyopathy by Inhibition of Adenylyl CyclaseR01HL095888 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI VATNER, DOROTHY EILEEN · 2009 to 2014
$1.7M
AC5 Inhibitor Treatment for Heart FailureP20HL101420 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI VATNER, STEPHEN F · 2010 to 2011
$1.6M
Age and Gender Differences in Apoptosis and Stem CellsR01AG023137 · NIA · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI VATNER, DOROTHY EILEEN · 2004 to 2008
$1.5M
CARDIOVASCULAR CONTROL IN NORMAL AND DISEASE STATESR37HL033107 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI VATNER, STEPHEN F · 1992 to 2001
$1.2M
NHLBI NIH HHS HL033107NHLBI NIH HHS HL069020NHLBI NIH HHS HL069752NHLBI NIH HHS HL093481NHLBI NIH HHS HL095888NHLBI NIH HHS HL101420NHLBI NIH HHS HL102472NHLBI NIH HHS P01 HL059139NHLBI NIH HHS P01 HL069020NHLBI NIH HHS P20 HL101420NHLBI NIH HHS R01 HL033107NHLBI NIH HHS R01 HL065183NHLBI NIH HHS R01 HL093481NHLBI NIH HHS R01 HL095888NHLBI NIH HHS R01 HL102472NHLBI NIH HHS R37 HL033107NHLBI NIH HHS T32 HL069752NIA NIH HHS AG027211NIA NIH HHS P01 AG027211NIA NIH HHS R01 AG014121NIA NIH HHS R01 AG023137NIA NIH HHS R01 AG028854
6 · The paper itself

Abstract

Despite remarkable advances in therapy, heart failure remains a leading cause of morbidity and mortality. Although enhanced beta-adrenergic receptor stimulation is part of normal physiologic adaptation to either the increase in physiologic demand or decrease in cardiac function, chronic beta-adrenergic stimulation has been associated with increased mortality and morbidity in both animal models and humans. For example, overexpression of cardiac Gsalpha or beta-adrenergic receptors in transgenic mice results in enhanced cardiac function in young animals, but with prolonged overstimulation of this pathway, cardiomyopathy develops in these mice as they age. Similarly, chronic sympathomimetic amine therapy increases morbidity and mortality in patients with heart failure. Conversely, the use of beta-blockade has proven to be of benefit and is currently part of the standard of care for heart failure. It is conceivable that interrupting distal mechanisms in the beta-adrenergic receptor-G protein-adenylyl cyclase pathway may also provide targets for future therapeutic modalities for heart failure. Interestingly, there are two major isoforms of adenylyl cyclase (AC) in the heart (type 5 and type 6), which may exert opposite effects on the heart, i.e., cardiac overexpression of AC6 appears to be protective, whereas disruption of type 5 AC prolongs longevity and protects against cardiac stress. The goal of this review is to summarize the paradigm shift in the treatment of heart failure over the past 50 years from administering sympathomimetic amine agonists to administering beta-adrenergic receptor antagonists, and to explore the basis for a novel therapy of inhibiting type 5 AC.

Indexed as

LongevitySignal TransductionAdenylyl CyclasesAge FactorsAgingApoptosisCardiotonic AgentsCyclic AMPFibrosisHeart FailureHumansMyocytes, CardiacReceptors, Adrenergic, betaRisk FactorsSarcoplasmic ReticulumSarcoplasmic Reticulum Calcium-Transporting ATPasesAdenylyl Cyclasesadenylyl cyclase type VCardiotonic AgentsCyclic AMPReceptors, Adrenergic, betaSarcoplasmic Reticulum Calcium-Transporting ATPases

Identifiers

PMID20658186
PMCPMC3655553
OpenAlexW2084078952

What OpenQuestion holds

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LicenceTDM
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.