Advances in incretin therapies for targeting cardiovascular disease in diabetes

IF 4.9 2区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
Timothy D. Roberts , Dana S. Hutchinson , Denise Wootten , Miles J. De Blasio , Rebecca H. Ritchie
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Abstract

The global prevalence of obesity is skyrocketing at an alarming rate, with recent data estimating that one-in-eight people are now living with the disease. Obesity is a chronic metabolic disorder that shares underlying pathophysiology with other metabolically-linked diseases such as type 2 diabetes mellitus, cardiovascular disease and diabetic cardiomyopathy. There is a distinct correlation between type 2 diabetes status and the likelihood of heart failure. Of note, there is an apparent sexual dimorphism, with women disproportionately affected with respect to the degree of severity of the cardiac phenotype of diabetic cardiomyopathy that results from diabetes. The current pharmacotherapies available for the attenuation of hyperglycaemia in type 2 diabetes are not always effective, and have varying degrees of efficacy in the setting of heart failure. Insulin can worsen heart failure prognosis whereas metformin, sodium-glucose cotransporter 2 inhibitors (SGLT2i) and more recently, glucagon-like peptide-1 receptor agonists (GLP-1RAs), have demonstrated cardioprotection with their administration. This review will highlight the advancement of incretin therapies for individuals with diabetes and heart failure and explore newly-reported evidence of the clinical usefulness of GLP-1R agonists in this distinct phenotype of heart failure.

Abstract Image

全球肥胖症发病率正以惊人的速度飙升,最新数据估计,现在每八人中就有一人患有肥胖症。肥胖症是一种慢性代谢性疾病,与其他代谢相关疾病(如 2 型糖尿病、心血管疾病和糖尿病心肌病)具有相同的潜在病理生理学。2 型糖尿病状态与心力衰竭的可能性之间存在明显的相关性。值得注意的是,在糖尿病导致的糖尿病心肌病心脏表型的严重程度方面,女性受影响的比例明显高于男性。目前可用于减轻 2 型糖尿病患者高血糖症状的药物疗法并不总是有效的,在心力衰竭的情况下也有不同程度的疗效。胰岛素会加重心力衰竭的预后,而二甲双胍、钠-葡萄糖共转运体 2 抑制剂(SGLT2i)和最近的胰高血糖素样肽-1 受体激动剂(GLP-1RAs)则显示出了对心脏的保护作用。本综述将重点介绍针对糖尿病合并心力衰竭患者的增量素疗法的进展,并探讨新近报道的 GLP-1R 激动剂在心力衰竭这一独特表型中的临床应用证据。
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来源期刊
CiteScore
10.70
自引率
0.00%
发文量
171
审稿时长
42 days
期刊介绍: The Journal of Molecular and Cellular Cardiology publishes work advancing knowledge of the mechanisms responsible for both normal and diseased cardiovascular function. To this end papers are published in all relevant areas. These include (but are not limited to): structural biology; genetics; proteomics; morphology; stem cells; molecular biology; metabolism; biophysics; bioengineering; computational modeling and systems analysis; electrophysiology; pharmacology and physiology. Papers are encouraged with both basic and translational approaches. The journal is directed not only to basic scientists but also to clinical cardiologists who wish to follow the rapidly advancing frontiers of basic knowledge of the heart and circulation.
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