Evidence map›Paper›PMID 24145181›Full record

ReviewJournal of cardiovascular pharmacology2014

Alpha-1-adrenergic receptors in heart failure: the adaptive arm of the cardiac response to chronic catecholamine stimulation.

Brian C Jensen, Timothy D OʼConnell, Paul C Simpson

Abstract readReview
In one paragraph

Review in Journal of cardiovascular pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
1.9field-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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Heart-rate response to alphaClinical autonomic research : official journal of the Clinical Autonomic Research Society · 2017
    Trial
  3. Article
  4. Article
  5. Article
  6. The Role of αBulletin of experimental biology and medicine · 2025
    Article
  7. Article
  8. Review
  9. Article
  10. A (AlphaJACC. Basic to translational science · 2024
    Article
  11. Article
  12. Article
  13. Mild allergic airways responses to an environmental mixture increase cardiovascular risk in rats.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Article
  14. Article
  15. Antifatigue Effect ofFrontiers in nutrition · 2022
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

3 authors at 1 institution in 1 country.

Brian C Jensen*Division of Cardiology and McAllister Heart Institute, University of North Carolina, Chapel Hill, NC; †Department of Integrative Biology and Physiology, University of Minnesota, Minneapolis, MN; and ‡Division of Cardiology, VA Medical Center, Cardiovascular Research Institute, and Department of Medicine, University of California, San Francisco, CA.
Timothy D OʼConnell
Paul C Simpson
University of Minnesota · US

Funding

The ubiquitin-proteasome system in cardiac remodelingP20RR017662 · NCRR · UNIVERSITY OF SOUTH DAKOTA · PI HARMON, ERIN B · 2002 to 2011
$18.7M
CATECHOLAMINES AND HYPERTROPHY OF CULTURED HEART CELLSR01HL031113 · NHLBI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI SIMPSON, PAUL C · 1985 to 2021
$5.7M
Alpha-1-Adrenergic Receptor Subtypes in the Cells of the Human HeartK08HL096836 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI JENSEN, BRIAN C · 2009 to 2013
$663k
Novel therapy for cardiotoxicity of cancer drugsI01BX001970 · VA · VETERANS AFFAIRS MED CTR SAN FRANCISCO · PI SIMPSON, PAUL C · 2013 to 2016
–
BLRD VA I01 BX001970NCRR NIH HHS P20 RR-017662NCRR NIH HHS P20 RR017662NHLBI NIH HHS HL31113NHLBI NIH HHS K08 HL096836NHLBI NIH HHS K08HL096836NHLBI NIH HHS R01 HL031113
6 · The paper itself

Abstract

Alpha-1-adrenergic receptors (ARs) are G protein-coupled receptors activated by catecholamines. The alpha-1A and alpha-1B subtypes are expressed in mouse and human myocardium, whereas the alpha-1D protein is found only in coronary arteries. There are far fewer alpha-1-ARs than beta-ARs in the nonfailing heart, but their abundance is maintained or increased in the setting of heart failure, which is characterized by pronounced chronic elevation of catecholamines and beta-AR dysfunction. Decades of evidence from gain and loss-of-function studies in isolated cardiac myocytes and numerous animal models demonstrate important adaptive functions for cardiac alpha-1-ARs to include physiological hypertrophy, positive inotropy, ischemic preconditioning, and protection from cell death. Clinical trial data indicate that blocking alpha-1-ARs is associated with incident heart failure in patients with hypertension. Collectively, these findings suggest that alpha-1-AR activation might mitigate the well-recognized toxic effects of beta-ARs in the hyperadrenergic setting of chronic heart failure. Thus, exogenous cardioselective activation of alpha-1-ARs might represent a novel and viable approach to the treatment of heart failure.

Indexed as

Adrenergic alpha-1 Receptor AntagonistsAnimalsCatecholaminesHeartHeart FailureHumansMiceMice, KnockoutReceptors, Adrenergic, alpha-1Adrenergic alpha-1 Receptor AntagonistsCatecholaminesReceptors, Adrenergic, alpha-1

Identifiers

PMID24145181
PMCPMC3980029
OpenAlexW2328568241

What OpenQuestion holds

Textmetadata
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.