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Chronic Neuregulin-1? Treatment Mitigates the Progression of Post-Myocardial
Infarction Heart Failure in the Setting of Type 1 Diabetes Mellitus by
Suppressing Myocardial Apoptosis, Fibrosis and Key Oxidant-Producing Enzymes.
Gupte M, Lal H, Ahmad F, Sawyer DB, Hill MF
Michael Hill on 9/26/2017
Journal of cardiac failure
Volume : Pages
Type 1 diabetes mellitus (DM) patients surviving myocardial infarction (MI) have
substantially higher cardiovascular morbidity and mortality compared to their
non-diabetic counterparts owing to the more frequent development of subsequent
heart failure (HF). Neuregulin (NRG)-1ß is released from cardiac microvascular
endothelial cells and acts as a paracrine factor via the ErbB family of tyrosine
kinase receptors expressed in cardiac myocytes to regulate cardiac development
and stress responses. Since myocardial NRG-1/ErbB signaling has been documented
to be impaired during HF associated with type 1 DM, we examined whether
enhancement of NRG-1ß signaling via exogenous administration of recombinant
NRG-1ß could exert beneficial effects against post-MI HF in the type 1 diabetic
heart., Type 1 DM was induced in male Sprague Dawley rats by a single injection
of streptozotocin (STZ) (65 mg/kg). Two weeks after induction of type 1 DM, rats
underwent left coronary artery ligation to induce MI. STZ-diabetic rats were
treated with saline or NRG-1ß (100 ug/kg) twice a week for 7 weeks, starting two
weeks prior to experimental MI. Residual left ventricular (LV) function was
significantly greater in the NRG-1ß-treated STZ-diabetic MI group compared to
the vehicle-treated STZ-diabetic MI group 5 weeks after MI as assessed by
high-resolution echocardiography. NRG-1ß treatment of STZ-diabetic MI rats was
associated with reduced myocardial fibrosis and apoptosis as well as decreased
gene expression of key oxidant-producing enzymes., These results suggest that
recombinant NRG-1ß may be a promising therapeutic for HF post-MI in the setting
of type 1 DM.
Neuropathy & Neurocognition
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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