Neuregulin‑1: An underlying protective force of cardiac dysfunction in sepsis (Review).

Abstract:

:Neuregulin-1 (NRG-1) is a type of epidermal growth factor‑like protein primarily distributed in the nervous and cardiovascular systems. When sepsis occurs, the incidence of cardiac dysfunction in myocardial injury is high and the mechanism is complicated. It directly causes myocardial cell damage, whilst also causing damage to the structure and function of myocardial cells, weakening of endothelial function and coronary microcirculation, autonomic dysfunction, and activation of myocardial inhibitory factors. Studies investigating NRG‑1 have been performed using a variety of methods, including in vitro models, and animal and human clinical trials; however, the results are not consistent. NRG‑1/ErbBs signaling is involved in a variety of cardiac processes, from the development of the myocardium and cardiac conduction systems to the promotion of angiogenesis in cardiomyocytes, and in cardio‑protective effects during injury. NRG‑1 may exert a multifaceted cardiovascular protective effect by activating NRG‑1/ErbBs signaling and regulating multiple downstream signaling pathways, thereby improving myocardial cell dysfunction in sepsis, and protecting cardiomyocytes and endothelial cells. It may alleviate myocardial microvascular endothelial injury in sepsis; its anti‑inflammatory effects inhibit the production of myocardial inhibitory factors in sepsis, improve myocardial ischemia, decrease oxidative stress, regulate the disruption to the homeostasis of the autonomic nervous system, improve diastolic function, and offer protective effects at multiple target sites. As the mechanism of action of NRG‑1 intersects with the pathways involved in the pathogenesis of sepsis, it may be applicable as a treatment strategy to numerous pathological processes in sepsis.

journal_name

Mol Med Rep

authors

Kang W,Cheng Y,Wang X,Zhou F,Zhou C,Wang L,Zhong L

doi

10.3892/mmr.2020.11034

subject

Has Abstract

pub_date

2020-06-01 00:00:00

pages

2311-2320

issue

6

eissn

1791-2997

issn

1791-3004

journal_volume

21

pub_type

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