Evidence map›Paper›PMID 31061918›Full record

ArticleJACC. Basic to translational science2019

Glucagon Receptor Antagonism Ameliorates Progression of Heart Failure.

Chen Gao, Shuxun Vincent Ren, Junyi Yu, Ulysis Baal, Dung Thai, John Lu, Chunyu Zeng, Hai Yan, Yibin Wang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JACC. Basic to translational science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Contractile Effects of Glucagon in Mouse Cardiac Preparations.International journal of molecular sciences · 2025
    Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Glucagon and Its Receptors in the Mammalian Heart.International journal of molecular sciences · 2023
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

9 authors.

Chen GaoDepartment of Anesthesiology, Cardiovascular Research Laboratories, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California.
Shuxun Vincent RenDepartment of Anesthesiology, Cardiovascular Research Laboratories, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California.
Junyi YuDepartment of Anesthesiology, Cardiovascular Research Laboratories, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California.
Ulysis BaalDepartment of Anesthesiology, Cardiovascular Research Laboratories, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California.
Dung ThaiREMD Biotherapeutics, Camarillo, California.
John LuREMD Biotherapeutics, Camarillo, California.
Chunyu ZengDepartment of Cardiology, Daping Hospital, The Third Military Medical University, Chongqing, China.
Hai YanREMD Biotherapeutics, Camarillo, California.
Yibin WangDepartment of Anesthesiology, Cardiovascular Research Laboratories, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California.

Funding

BCAA Catabolic Defect in HF: Novel Mechanism and Therapeutic TargetR01HL140116 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LI, ZHAOPING · 2018 to 2021
$1.6M
NHLBI NIH HHS R01 HL140116
6 · The paper itself

Abstract

Mice were treated with a fully human monoclonal glucagon receptor antagonistic antibody REMD2.59 following myocardial infarction or pressure overload. REMD2.59 treatment blunted cardiac hypertrophy and fibrotic remodeling, and attenuated contractile dysfunction at 4 weeks after myocardial infarction. In addition, REMD2.59 treatment at the onset of pressure overload significantly suppressed cardiac hypertrophy and chamber dilation with marked preservation of cardiac systolic and diastolic function. Initiation of REMD2.59 treatment 2 weeks after pressure overload significantly blunted the progression of cardiac pathology. These results provide the first in vivo proof-of-concept evidence that glucagon receptor antagonism is a potentially efficacious therapy to ameliorate both onset and progression of heart failure.

Indexed as

GCGR, glucagon receptorGLC, glucagonglucagon receptor antagonismheart failureMI, myocardial infarctionmyocardial infarctionPBS, phosphate-buffered salinePCR, polymerase chain reactionpressure overloadTAC, transaortic constriction

Identifiers

PMID31061918
PMCPMC6488764

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.