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Review
. 2015 Apr 8;10(Suppl 1):1-9.
doi: 10.4137/BMI.S20061. eCollection 2015.

The roles of neuregulin-1 in cardiac development, homeostasis, and disease

Cassady E Rupert  1 , Kareen Lk Coulombe  2
Affiliations
Review

The roles of neuregulin-1 in cardiac development, homeostasis, and disease

Cassady E Rupert et al. Biomark Insights. .

Abstract

Neuregulin-1 (NRG-1) and its signaling receptors, erythroblastic leukemia viral oncogene homologs (ErbB) 2, 3, and 4, have been implicated in both cardiomyocyte development and disease, as well as in homeostatic cardiac function. NRG-1/ErbB signaling is involved in a multitude of cardiac processes ranging from myocardial and cardiac conduction system development to angiogenic support of cardiomyocytes, to cardioprotective effects upon injury. Numerous studies of NRG-1 employ a variety of platforms, including in vitro assays, animal models, and human clinical trials, with equally varying and, sometimes, contradictory outcomes. NRG-1 has the potential to be used as a therapeutic tool in stem cell therapies, tissue engineering applications, and clinical diagnostics and treatment. This review presents a concise summary of the growing body of literature to highlight the temporally persistent significance of NRG-1/ErbB signaling throughout development, homeostasis, and disease in the heart, specifically in cardiomyocytes.

Keywords: ErbB receptors; cardiac regeneration; cardiomyocyte; neuregulin-1; stem cells; therapeutic.

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Figures

Figure 1
Figure 1
NRG-1/ErbB signaling has diverse, context-dependent physiological effects in the heart during development, homeostasis, and disease. Notes: Upon binding of NRG-1 to its ErbB3/4 receptor, dimerization with another ErbB2 (preferred), ErbB3, or ErbB4 receptor initiates a cascade of downstream signals in the heart. Signaling plays an important role in the following: development of the ventricular wall, arteriovenous (AV) valves, and the cardiac conduction system; homeostatic function of the heart via cardiomyocyte adaptability to stress and microvascular support; and the adaptation to disease such as myocardial infarction (MI) in both acute and chronic heart failure (CHF), as reflected by changes in left ventricular ejection fraction (LVEF).
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