Evidence map›Paper›PMID 29871977›Full record

ArticleCirculation2018

Multiprotein Complex With TRPC (Transient Receptor Potential-Canonical) Channel, PDE1C (Phosphodiesterase 1C), and A2R (Adenosine A2 Receptor) Plays a Critical Role in Regulating Cardiomyocyte cAMP and Survival.

Yishuai Zhang, Walter Knight, Si Chen, Amy Mohan, Chen Yan

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Circulation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Phosphodiesterases: Evolving Concepts and Implications for Human Therapeutics.Annual review of pharmacology and toxicology · 2025
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Cyclic GMP and PKG Signaling in Heart Failure.Frontiers in pharmacology · 2022
    Review
  17. Review
  18. PDE1 Inhibition Modulates CaCirculation research · 2021
    Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Yishuai ZhangAab Cardiovascular Research Institute, Department of Medicine (Y.Z., W.K., S.C., A.M., C.Y.), University of Rochester School of Medicine and Dentistry, NY.
Walter KnightAab Cardiovascular Research Institute, Department of Medicine (Y.Z., W.K., S.C., A.M., C.Y.), University of Rochester School of Medicine and Dentistry, NY.
Si ChenAab Cardiovascular Research Institute, Department of Medicine (Y.Z., W.K., S.C., A.M., C.Y.), University of Rochester School of Medicine and Dentistry, NY.
Amy MohanAab Cardiovascular Research Institute, Department of Medicine (Y.Z., W.K., S.C., A.M., C.Y.), University of Rochester School of Medicine and Dentistry, NY.
Chen YanAab Cardiovascular Research Institute, Department of Medicine (Y.Z., W.K., S.C., A.M., C.Y.), University of Rochester School of Medicine and Dentistry, NY.
University of Rochester · USCardiovascular Research Center · BRYoung Invincibles · US

Funding

Regulation and Function of Phosphodiesterase in the HeartR01HL088400 · NHLBI · UNIVERSITY OF ROCHESTER · PI YAN, CHEN · 2008 to 2018
$3.1M
PDE10A Regulation and Function in Cardiovascular DiseaseR01HL134910 · NHLBI · UNIVERSITY OF ROCHESTER · PI BERK, BRADFORD C, YAN, CHEN · 2017 to 2020
$2.1M
NHLBI NIH HHS R01 HL088400NHLBI NIH HHS R01 HL134910
6 · The paper itself

Abstract

backgroundcAMP plays a critical role in regulating cardiomyocyte survival. Various cAMP signaling pathways behave distinctly or in opposition. We have previously reported that activation of cAMP hydrolysis by cyclic nucleotide phosphodiesterase 1C (PDE1C) promotes cardiomyocytes death/apoptosis, yet the underlying molecular mechanism remains unknown. In this study, we aimed to identify the specific cAMP signaling pathway modulated by PDE1C and determine the mechanism by which Ca

methodsTo study cardiomyocyte death/apoptosis, we used both isolated mouse adult cardiomyocytes in vitro and doxorubicin-induced cardiotoxicity in vivo. We used a variety of pharmacological activators and inhibitors as well as genetically engineered molecular tools to manipulate the expression and activity of proteins of interest.

resultsWe found that the protective effect of PDE1C inhibition/deficiency on Ang II or doxorubicin-induced cardiomyocyte death/apoptosis is dependent on cAMP-generating adenosine A

conclusionsWe have characterized a novel multiprotein complex comprised of A

Indexed as

Adenosine A2 Receptor AntagonistsAngiotensin IIAnimalsApoptosisCalcium SignalingCell SurvivalCyclic AMPCyclic Nucleotide Phosphodiesterases, Type 1DoxorubicinFemaleMaleMiceMice, Inbred C57BLMice, KnockoutMyocytes, CardiacReceptors, Adenosine A2Adenosine A2 Receptor AntagonistsAngiotensin IICyclic AMPCyclic Nucleotide Phosphodiesterases, Type 1DoxorubicinPde1C protein, mouseReceptors, Adenosine A2RNA, Small InterferingTRPC3 cation channelTRPC Cation Channelsadenosine signalingcAMPcardiomyocyte deathcardiotoxicityphosphodiesterase

Identifiers

PMID29871977
PMCPMC6205915
OpenAlexW2899480454

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.