Integrative Analysis of Key Genes and Signaling Pathways By Bioinformatics in Patients with Type 1 Diabetes Mellitus Combined with Acute Myocardial Infarction

Type 1 Diabetes ◽

Signaling Pathways ◽

Human Genes ◽

Novel Biomarkers ◽

Key Genes

Abstract Although the pathogenesis of type 1 diabetes mellitus (T1D) and acute myocardial infarction (AMI) remains unclear. We investigated the key genes and signaling pathways common to T1D and AMI. First, we screened differentially expressed genes (DEGs) co-expressed by T1D and AMI through gene expression synthesis (GEO) database and text mining. David database was used for enrichment and functional analysis of selected genes. The interaction between proteins (PPI) was created using STRING and Cytoscape software. MCODE is used for module analysis of PPI network. A total of 74 human genes that met the criteria were found in T1D and AMI. The first 10 central genes include STAT3, ITGAM, MMP9, ERBB2, MAPK3, FOS, MYD88, MAPK1, TFRC and TNFRSF1A.The establishment of the aforementioned key genes might serve as novel biomarkers for precision diagnosis and providing medical treatment for the occurrence of AMI in T1D patients in the future.

Type 1 Diabetes Mellitus Following Acute Myocardial Infarction in a Young Adult

Internal Medicine ◽

10.2169/internalmedicine.44.897 ◽

2005 ◽

Vol 44 (8) ◽

pp. 897-898

Author(s):

Toshio KAHARA ◽

Yoshiki NAGATA ◽

Hiroshi AKAHORI ◽

Rika USUDA

Keyword(s):

Diabetes Mellitus ◽

Myocardial Infarction ◽

Type 1 Diabetes ◽

Young Adult ◽

Type 1 Diabetes Mellitus

Fluminant Type 1 Diabetes Mellitus with Acute Myocardial Infarction Caused by Coronary Vasospasm

Nihon Naika Gakkai Zasshi ◽

10.2169/naika.98.1708 ◽

2009 ◽

Vol 98 (7) ◽

pp. 1708-1710

Author(s):

Kenji Honkura ◽

Rika Yamashita ◽

Michinori Takahashi ◽

Kazuro Kaise ◽

Jin Seino ◽

...

Keyword(s):

Diabetes Mellitus ◽

Myocardial Infarction ◽

Type 1 Diabetes ◽

Coronary Vasospasm

Abstract #289: In-Hospital Mortality in Patients Admitted for Acute Myocardial Infarction: Type 1 Diabetes Mellitus Compared to Type 2 Diabetes Mellitus

Endocrine Practice ◽

10.1016/s1530-891x(20)44409-x ◽

2017 ◽

Vol 23 ◽

pp. 79-80

Author(s):

Franco Vallejo ◽

Carolina Hurtado ◽

Katherine Lopez ◽

Rodrigo Garcia ◽

Jeanine Albu

Keyword(s):

Diabetes Mellitus ◽

Myocardial Infarction ◽

Type 2 Diabetes ◽

Type 1 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Hospital Mortality ◽

Type 1 Diabetes Mellitus

Multi-Organ Protective Effects of Curcumin Nanoparticles on Drug-Induced Acute Myocardial Infarction in Rats with Type 1 Diabetes Mellitus

Applied Sciences ◽

10.3390/app11125497 ◽

2021 ◽

Vol 11 (12) ◽

pp. 5497

Author(s):

Paul-Mihai Boarescu ◽

Ioana Boarescu ◽

Adriana Elena Bulboacă ◽

Ioana Corina Bocșan ◽

Raluca Maria Pop ◽

...

Keyword(s):

Diabetes Mellitus ◽

Myocardial Infarction ◽

Type 1 Diabetes ◽

Kidney Tissue ◽

Control Group ◽

Protective Effects ◽

Drug Induced

The objectives of this study were to investigate the cardio-protective, hepatoprotective and nephroprotective effects of curcumin nanoparticle (NC) pretreatment compared to conventional curcumin (CC) on acute myocardial infarction (AMI) in rats with type 1 diabetes mellitus (T1DM). Fifty-six Wister Bratislava rats were divided into eight groups. The first four groups—C (control group), AMI (group with AMI), T1DM (group with T1DM), and T1DM-AMI (group with T1DM and AMI)—received only saline (S) during the whole experiment. Two groups—S-T1DM-CC-AMI and S-T1DM-NC-AMI—were pretreated with S before T1DM induction. The S-T1DM-CC-AMI group received CC (200 mg/Kg bw (bw—body weight)) after T1DM induction, while the S-T1DM-NC-AMI group received NC (200 mg/Kg bw) after T1DM induction. the CC-T1DM-CC-AMI group received CC (200 mg/Kg bw) during the whole experiment. Similarly, the NC-T1DM-NC-AMI group received NC (200 mg/Kg bw) over the entire experiment. T1DM was induced on day 7 using a single dose of streptozotocin (STZ). AMI was induced with isoproterenol (ISO) on day 22. Both curcumin formulations, CC and NC, prevented the following electrocardiographic changes: prolongation of the QRS complex, enlargement of QT and QTc intervals, and ST-segment elevation. Glucose levels and lipid profile parameters were reduced up to 1.9 times, while C-peptide serum levels were increased up to 1.6 times in groups that received CC or NC. Liver function parameters (aspartate transaminase, alanine transaminase) and kidney function parameters (creatinine, urea) were reduced 4.8 times, and histological changes of liver and kidney tissue were improved by CC or NC administration. Pretreatment with NC proved significantly higher cardioprotective, hepatoprotective and nephroprotective effects in the case of AMI in T1DM.

Abstract 352: Myocardial Neuregulin-1/ErbB Signaling Is Impaired in the Setting of Post--Myocardial Infarction Heart Failure Complicated by Type 1 Diabetes Mellitus

Circulation Research ◽

10.1161/res.111.suppl_1.a352 ◽

2012 ◽

Vol 111 (suppl_1) ◽

Author(s):

Oghenerukevwe Odiete ◽

Kathleen E Dennis ◽

Douglas B Sawyer ◽

Michael F Hill

Keyword(s):

Diabetes Mellitus ◽

Myocardial Infarction ◽

Heart Failure ◽

Type 1 Diabetes ◽

Protein Expression ◽

Neuregulin 1 ◽

Erbb Signaling ◽

Type 1 Dm

Background: Type 1 diabetes mellitus (DM) patients surviving myocardial infarction (MI) are at heightened risk for the subsequent development of heart failure (HF). Despite the worse outcomes, investigations into the pathophysiological mechanisms that contribute to the increased frequency of HF after MI in the type 1 DM heart remain scarce. Neuregulin-1 (NRG-1), along with the ErbB family of receptor tyrosine kinases through which NRG-1 ligands signal, have been shown to be intimately involved in mediating cardiac recovery after MI. However, the impact of type 1 DM on this signaling system post-MI remains to be elucidated. Therefore, in the present study, we examined myocardial NRG-1/ErbB signaling during post-MI HF in the presence of type 1 DM. Methods: Type 1 DM was induced in male Sprague-Dawley rats via a single intraperitoneal injection of streptozotocin (STZ) (65 mg/kg). Two weeks after induction of type 1 DM, MI was produced in DM and non-DM rats by ligation of the left anterior descending (LAD) coronary artery. Residual left ventricular (LV) function was assessed by echocardiography at 4 weeks post-MI. Following echocardiographic assessment, NRG-1, ErbB2, and ErbB4 protein expression was assessed in the remote, surviving LV myocardium of DM and non-DM rats using Western blot techniques. Results: LV Fractional Shortening (FS) and LV Ejection Fraction (EF) were significantly lower in the DM + MI group compared to the MI group ([LVFS: DM + MI, 17.9 ± 0.7 (n=6) vs. MI, 25.2 ± 2.2 (n=6), p <0.05; LVEF: DM + MI, 35.5 ± 1.4 (n=6) vs. MI, 47.5 ± 3.5 (n=6), p <0.05]), indicating an increased functional severity of HF in the diabetic post-MI group. The weight of myocardial scar caused by the infarction was not significantly different between the MI groups ([DM + MI, 0.19 ± 0.02 g (n=4) vs. MI, 0.20 ± 0.03 g (n=4), p =0.70]). ErbB2, ErbB4, and NRG-1 protein expression levels were all significantly lower in the DM + MI group compared to the MI group. Conclusions: These findings demonstrate that type 1 DM impairs myocardial NRG-1/ErbB signaling in response to MI, which may contribute to the accelerated progression of subsequent HF. Augmentation of NRG-1 or its downstream signaling pathways may represent a novel therapeutic strategy for ameliorating post-MI HF in the setting of type 1 DM.