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Cited by 68Receptor Mechanisms and SignalingPhosphodiesterase function and regulationHeart Failure Treatment and Management

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

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Ho, David, Yan, Lin, Iwatsubo, Kousaku, Vatner, Dorothy E., Vatner, Stephen F.·2010·Heart Failure Reviews
DOI 10.1007/s10741-010-9183-5PMC PMC3655553
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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.

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  • Top enriched pathways for hypertrophic cardiomyopathy pointed to candidate cardiomyocyte-specific therapeutic targets including ADCY5 and druggable targets including SRPK3.

    “Top enriched pathways for hypertrophic cardiomyopathy pointed to candidate cardiomyocyte-specific therapeutic targets including ADCY5, disruption of which is associated with longevity and protection against cardiomyopathy in mouse models40, as well as druggable targets41 including SRPK3, a downstream effector of MEF242 which is known to play a critical role in myocardial cell hypertrophy43.”

    From Transfer learning enables predictions in network biology (2023) · cites this paper as [40]

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Authors
Ho, D., Yan, L., Iwatsubo, K., Vatner, D. E., & Vatner, S. F.
Affiliations
Rutgers New Jersey Medical School (US)
Corresponding author
Vatner, Stephen F.
ORCID
Venue
Heart Failure Reviews
Publisher
Springer Science and Business Media LLC
Published
2010-07-24
Volume
15
Issue
5
Pages
495-512
ISSN
  • 1382-4147 (ISSN-L)
  • 1573-7322
DOI
10.1007/s10741-010-9183-5
PMC
PMC3655553
OpenAlex
W2084078952
Cited by
68
References
230
Citations by year
2025: 1 · 2024: 3 · 2023: 6 · 2022: 3 · 2021: 2 · 2020: 3 · 2019: 5 · 2018: 4 · 2017: 6 · 2016: 5 · 2015: 7 · 2014: 3 · 2013: 10 · 2012: 7
FWCI
0.56
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • Heart Failure Reviews (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (6t32hl069752-11)
  • National Institute on Aging (AG027211, R01AG023137, R01AG014121, R01AG028854, P01AG027211)
  • National Heart, Lung, and Blood Institute (P20HL101420, HL-033107, HL095888, HL-093481, R37HL033107, HL069020, R01HL065183, P01HL059139, HL102472, R01HL095888, HL101420, R01HL102472, R01HL033107, P01HL069020, R01HL093481, T32-HL069752, HL-069752)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Phosphodiesterase function and regulation
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Failure Treatment and Management
Keywords
heart failure, beta-adrenergic signaling, adenylyl cyclase type 5, beta-adrenergic blockade, cardiomyopathy, longevity, adenylate cyclase inhibition
MeSH terms
Cyclic AMP, Adenylyl Cyclases, Age Factors, Aging, Cardiotonic Agents, Fibrosis, Heart Failure, Humans, Longevity, Receptors, Adrenergic, beta, Risk Factors, Sarcoplasmic Reticulum, Signal Transduction, Apoptosis, Myocytes, Cardiac, Sarcoplasmic Reticulum Calcium-Transporting ATPases

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