ArticleExperimental and therapeutic medicine2013
Gene transfer of human neuregulin-1 attenuates ventricular remodeling in diabetic cardiomyopathy rats.
Article in Experimental and therapeutic medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- The role of myocardial fibrosis in the diabetic cardiomyopathy.Diabetology & metabolic syndrome · 2025Review
- Expression and secretion of neuregulin-1 in cardiac microvascular endothelial cells treated with angiogenic factors.Experimental and therapeutic medicine · 2018Article
- Chronic Neuregulin-1β Treatment Mitigates the Progression of Postmyocardial Infarction Heart Failure in the Setting of Type 1 Diabetes Mellitus by Suppressing Myocardial Apoptosis, Fibrosis, and Key Oxidant-Producing Enzymes.Journal of cardiac failure · 2017Article
- Neuregulin-1 attenuates development of nephropathy in a type 1 diabetes mouse model with high cardiovascular risk.American journal of physiology. Endocrinology and metabolism · 2016Article
- Signalling between microvascular endothelium and cardiomyocytes through neuregulin.Cardiovascular research · 2014Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuregulin-1 (NRG-1) is a cardioactive growth factor released from endothelial cells. However, the effect of NRG-1 on ventricular remodeling in diabetic cardiomyopathy (DCM) remains unclear. The aim of the present study was to investigate the pathophysiological role of NRG-1 in a rat model of DCM. Rat cardiac microvascular endothelial cells (CMECs) were transfected with human NRG-1 (hNRG-1) lentivirus. The hNRG-1 medium was utilized to culture rat cardiomyocytes. The cardiomyocytes were counted with a hemacytometer to determine the proliferation index and Annexin V/propidium iodide double staining was employed to examine the apoptotic rate. A rat model of DCM was induced by an intraperitoneal injection of streptozotocin. The hNRG-1 lentivirus was injected into the myocardium of the DCM model rats. Four weeks after the lentiviral injection, cardiac catheterization was performed to evaluate the cardiac function. Apoptotic cells were determined by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining. Left ventricular sections were stained with Masson's trichrome to investigate the myocardial collagen content. The expression levels of related genes and proteins were analyzed. The results indicated that hNRG-1 conditioned medium stimulated the proliferation and counteracted the apoptosis of cardiomyocytes
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