Glucagon-like peptide-1 and its cardiovascular effects

Research output: Contribution to journalReview article

12 Citations (Scopus)

Abstract

Recently, the crucial role of GLP-1 in cardiovascular disease has been suggested by both preclinical and clinical studies. In vivo and in vitro studies have demonstrated cardio-protective effects of GLP-1 by activating cell survival signal pathways, which have greatly reduced ischemia/reperfusion injury and also cardiac dysfunction in various congestive heart failure animal models. Clinically, beneficial effects of GLP-1 have been shown in patients with myocardial infarction, hypertension, and heart failure, and 2 classes of incretin enhancers, GLP-1 receptor agonists and DPP-4 inhibitors, are currently available for the treatment of type 2 diabetes mellitus. In this review, we will summarize the role of incretins in various cardiovascular events such as hypertension and heart failure and postprandial lipoprotein secretion, and discuss their molecular mechanisms and potentials as a new therapeutic as well as preventive drug type for reducing cardiovascular events in both diabetic and nondiabetic patients.

Original languageEnglish (US)
Pages (from-to)422-428
Number of pages7
JournalCurrent atherosclerosis reports
Volume14
Issue number5
DOIs
StatePublished - Oct 1 2012

Fingerprint

Glucagon-Like Peptide 1
Incretins
Heart Failure
Hypertension
Cardiovascular Agents
Reperfusion Injury
Type 2 Diabetes Mellitus
Lipoproteins
Signal Transduction
Cell Survival
Cardiovascular Diseases
Animal Models
Myocardial Infarction
Therapeutics

Keywords

  • Cardiovascular disease
  • Dipeptidyl peptidase-4
  • Glucagon-like peptide-1
  • Glucagon-like peptide-1 receptor
  • Incretins
  • Myocardial infarction
  • Type 2 diabetesmellitus

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Glucagon-like peptide-1 and its cardiovascular effects. / Heo, Kyung Sun; Fujiwara, Keigi; Abe, Jun Ichi.

In: Current atherosclerosis reports, Vol. 14, No. 5, 01.10.2012, p. 422-428.

Research output: Contribution to journalReview article

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