Evidence map›Paper›PMID 26701329›Full record

ReviewHeart failure reviews2016

Partial adenosine A1 receptor agonism: a potential new therapeutic strategy for heart failure.

Stephen J Greene, Hani N Sabbah, Javed Butler, Adriaan A Voors, Barbara E Albrecht-Küpper, Hans-Dirk Düngen, Wilfried Dinh, Mihai Gheorghiade

Abstract readReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 60 citations in OpenAlex.

  1. Trial
  2. Adenosine AInternational journal of molecular sciences · 2024
    Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. AStructure (London, England : 1993) · 2021
    Article
  9. Frontiers in pharmacology · 2021
    Article
  10. Article
  11. Review
  12. Article
  13. AFrontiers in pharmacology · 2020
    Article
  14. Review
  15. Adenosine and the Cardiovascular System.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2019
    Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Review
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

8 authors at 7 institutions in 3 countries.

Stephen J GreeneDivision of Cardiology, Duke University Medical Center, Durham, NC, USA.
Hani N SabbahDivision of Cardiovascular Medicine, Department of Medicine, Henry Ford Hospital, Detroit, MI, USA.
Javed ButlerDivision of Cardiology, Stony Brook University, Stony Brook, NY, USA.
Adriaan A VoorsDepartment of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
Barbara E Albrecht-KüpperDepartments of Heart Diseases and Medicinal Chemistry, Bayer Pharma AG Research Center, Wuppertal, Germany.
Hans-Dirk DüngenDepartment of Cardiology, Campus Virchow, Charite Universitätsmedizin Berlin, Berlin, Germany.
Wilfried DinhDepartment of Cardiology, HELIOS Clinic Wuppertal, University Hospital Witten/Herdecke, Wuppertal, Germany.
Mihai GheorghiadeCenter for Cardiovascular Innovation, Northwestern University Feinberg School of Medicine, 201 East Huron, Galter 3-150, Chicago, IL, 60601, USA. m-gheorghiade@northwestern.edu.
Bayer (Germany) · DECharité - Universitätsmedizin Berlin · DEDuke Medical Center · USHenry Ford Hospital · USNorthwestern University · USStony Brook University · USUniversity of Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heart failure (HF) represents a global public health and economic problem associated with unacceptable rates of death, hospitalization, and healthcare expenditure. Despite available therapy, HF carries a prognosis comparable to many forms of cancer with a 5-year survival rate of ~50%. The current treatment paradigm for HF with reduced ejection fraction (EF) centers on blocking maladaptive neurohormonal activation and decreasing cardiac workload with therapies that concurrently lower blood pressure and heart rate. Continued development of hemodynamically active medications for stepwise addition to existing therapies carries the risk of limited tolerability and safety. Moreover, this treatment paradigm has thus far failed for HF with preserved EF. Accordingly, development of hemodynamically neutral HF therapies targeting primary cardiac pathologies must be considered. In this context, a partial adenosine A1 receptor (A1R) agonist holds promise as a potentially hemodynamically neutral therapy for HF that could simultaneous improve cardiomyocyte energetics, calcium homeostasis, cardiac structure and function, and long-term clinical outcomes when added to background therapies. In this review, we describe the physiology and pathophysiology of HF as it relates to adenosine agonism, examine the existing body of evidence and biologic rationale for modulation of adenosine A1R activity, and review the current state of drug development of a partial A1R agonist for the treatment of HF.

Indexed as

Heart FailureAdenosine A1 Receptor AgonistsCardiovascular AgentsDrug Partial AgonismHumansReceptor, Adenosine A1Stroke VolumeAdenosine A1 Receptor AgonistsCardiovascular AgentsReceptor, Adenosine A1AdenosineAdenosine A1 receptorHeart failureMitochondriaPartial agonistTherapy

Identifiers

PMID26701329
OpenAlexW2197759468

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.