scholarly journals Potential role of a disintegrin and metalloproteinase-17 (ADAM17) in age-associated ventricular remodeling of rats

RSC Advances ◽  
2019 ◽  
Vol 9 (25) ◽  
pp. 14321-14330 ◽  
Author(s):  
Hainiang Liu ◽  
Haoren Wang ◽  
Dong Cheng ◽  
Qinfu Wang ◽  
Zuowei Pei ◽  
...  
Keyword(s):  
Potential Role ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Tnf Α ◽  
A Disintegrin And Metalloproteinase ◽  
Factor Α ◽  
Necrosis Factor

Excessive tumor necrosis factor-α (TNF-α) could enhance cell death and aggravate left ventricular remodeling and myocardial dysfunction.

scholarly journals Predictors of left ventricular hypertrophy development in patients with essential hypertension: role of pro- and anti-inflammatory cytokines

2018 ◽  
Vol 2 (Issue 4) ◽  
pp. 97 ◽  
Author(s):  
Larisa Tsoi ◽  
Andrei Polupanov ◽  
Ibragim Sabirov ◽  
Tazagul Zalova ◽  
Flora Rysmatova
Keyword(s):  
Essential Hypertension ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Interleukin 10 ◽  
Left Ventricular ◽  
Myocardial Remodeling ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Objective: The data on the relationship between the level of TNF-α and interleukin-10 with the presence of left ventricular hypertrophy and myocardial remodeling in patients with essential hypertension is presented. Methods: Overall, 156 patients with essential hypertension aged 40 to 75 years (with mean age 55.8 ± 7.5 years) were examined; of which 57 were women and 99 were men. All patients were divided into two groups. The first group included 73 patients showing the presence of  left ventricular hypertrophy (LVH), established by echocardiography; the second group included 83 patients who showed no signs of LVH on the echocardiogram. Results: According to the study, no relationship was found between the concentration of tumor necrosis factor α (TNF-α) and the development of LVH. It was also shown that only men, but not women with, were associated with the presence of LVH with low levels of interleukin-10 ( IL-10). In addition, a negative correlation was found between the concentration of tumor necrosis factor α (TNF-α) and IL-10 with the thickness of the left ventricular walls at the initial stages of myocardial remodeling on the echocardiography. Conclusion: Thus, our study demonstrates the modulating role of inflammation on the processes of myocardial remodeling in hypertension.

Role of oxidative stress in left ventricular remodeling and heart failure after myocardial infarction

1999 ◽  
Vol 5 (3) ◽  
pp. 79
Author(s):  
Shintaro Kinugawa ◽  
Hiroyuki Tsutsui ◽  
Tomomi Ide ◽  
Hideo Ustumi ◽  
Nobuhiro Suematsu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular

The Role of Tumor Necrosis Factor-α (TNF-α) Polymorphisms in Gastric Cancer: a Meta-Analysis

2021 ◽  
Author(s):  
Maryam Gholamalizadeh ◽  
Samaneh Mirzaei Dahka ◽  
Hadi Sedigh Ebrahim-Saraie ◽  
Mohammad Esmail Akbari ◽  
Azam Pourtaheri ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Meta Analysis ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Abstract 865: Gata-4 Is An Angiogenic Survival Factor Of The Infarcted Heart

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Olli Tenhunen ◽  
Hanna Leskinen ◽  
Raisa Serpi ◽  
Jaana Rysä ◽  
Harri Pennanen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Stem Cells ◽  
Gene Transfer ◽  
Dna Binding ◽  
Ventricular Remodeling ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
Therapeutic Interventions ◽  
Cardiac Stem Cells

Recent data suggest that the cardiac-restricted transcription factor GATA-4 is an anti-apoptotic factor required for adaptive responses as well as a key regulator of hypertrophy and hypertrophy-associated genes in the heart. As a leading cause of chronic heart failure, reversal of post-infarction left ventricular remodeling represents an important target for therapeutic interventions. Here we studied the role of GATA-4 as a mediator of post-infarction remodeling. Rats were subjected to experimental myocardial infarction (MI) by ligating the left anterior descending coronary artery (LAD). Ligation of the LAD decreased the DNA binding activity of GATA-4 by 69 % at day 1 after MI (P<0.001, n=7– 8) as assessed by gel mobility shift assays. At 2 weeks the GATA-4 DNA binding was significantly upregulated (2.4-fold, P<0.05, n=7), and returned to baseline at 4 weeks. To determine the functional role of GATA-4, rats underwent LAD ligation followed by peri-infarct intramyocardial delivery of adenoviral vector expressing GATA-4. Hearts treated with the GATA-4 gene transfer exhibited significantly increased ejection fraction (58±5% vs. 38±3% in LacZ-treated control animals with MI, P<0.001, n=8 –9) and fractional shortening (28±3% vs. 16±1%, P<0.001, n=8 –9) 2 weeks after MI. Accordingly, the infarct size was significantly reduced (26±4% vs. 45±4%, P<0.01, n=8 –9). To determine the cardioprotective mechanisms of GATA-4, the number of cardiac stem cells, apoptotic cardiomyocytes and capillaries were assessed. The number of capillaries (59±4/field vs. 48±3/field, P<0.051, n=7– 8) and c-kit positive stem cells (13±5 cells vs. 4±2 cells, P<0.05, n=7– 8) were increased in GATA-4 treated hearts, and a tendency to decreased apoptosis was observed in TUNEL-stained histological sections. These results indicate that the reversal of reduced GATA-4 activity prevents adverse post-infarction remodeling through increased angiogenesis, recruitment of cardiac stem cells and anti-apoptosis. GATA-4-based gene transfer may represent a novel, efficient therapeutic approach for heart failure.

Metalloprotease-disintegrins: modular proteins capable of promoting cell-cell interactions and triggering signals by protein-ectodomain shedding

1999 ◽  
Vol 112 (21) ◽  
pp. 3603-3617 ◽  
Author(s):  
J. Schlondorff ◽  
C.P. Blobel
Keyword(s):  
Tumor Necrosis ◽  
Ectodomain Shedding ◽  
Membrane Glycoproteins ◽  
Tnf Α ◽  
Disintegrin Domain ◽  
Protein Ectodomain Shedding ◽  
Integrin Ligands ◽  
Factor Α ◽  
Necrosis Factor

Metalloprotease-disintegrins (ADAMs) have captured our attention as key players in fertilization and in the processing of the ectodomains of proteins such as tumor necrosis factor (α) (TNF(α)), and because of their roles in Notch-mediated signaling, neurogenesis and muscle fusion. ADAMs are integral membrane glycoproteins that contain a disintegrin domain, which is related to snake-venom integrin ligands, and a metalloprotease domain (which can contain or lack a catalytic site). Here, we review and critically discuss current topics in the ADAMs field, including the central role of fertilin in fertilization, the role of the TNF(α) convertase in protein ectodomain processing, the role of Kuzbanian in Notch signaling, and links between ADAMs and processing of the amyloid-precursor protein.

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