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Glucagon Receptor Antagonism Ameliorates Progression of Heart Failure.

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.

SUBMITTER: Gao C

PROVIDER: S-EPMC6488764 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

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Glucagon Receptor Antagonism Ameliorates Progression of Heart Failure.

Gao Chen C Ren Shuxun Vincent SV Yu Junyi J Baal Ulysis U Thai Dung D Lu John J Zeng Chunyu C Yan Hai H Wang Yibin Y

JACC. Basic to translational science 20190313 2

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 functio ...[more]

PMID: 31061918

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