scholarly journals Signaling Pathways of Cardiac Remodeling Related to Angiotensin II

10.5772/66076 ◽  
2017 ◽  
Author(s):  
Carolina Baraldi Araujo Restini ◽  
Arthur F. Engracia Garcia ◽  
Henrique Melo Natalin ◽  
Guilherme Melo Natalin ◽  
Elen Rizzi
Keyword(s):  
Angiotensin Ii ◽  
Signaling Pathways ◽  
Cardiac Remodeling

Abstract 3467: Fibulin-2 Enhances Angiotensin-II-Induced Transforming Growth Factor (TGF)-β Activation in Promoting Cardiac Remodeling in the Mouse Model I n Vivo

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Hangxiang Zhang ◽  
Hailong Dong ◽  
Jing Wu ◽  
Mon-Li Chu ◽  
Takeshi Tsuda
Keyword(s):  
Angiotensin Ii ◽  
Signaling Pathways ◽  
Cardiac Remodeling ◽  
Matrix Protein ◽  
Transforming Growth Factor ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Ang Ii ◽  
Downstream Signaling ◽  
Collagen Iii

Background: Angiotensin-II (Ang-II) is a potent neurohormone responsible for progression of cardiac remodeling in which TGF-β serves as a principal downstream mediator. In our previous study, genetic deletion of fibulin-2 attenuated progression of ventricular dysfunction after experimental myocardial infarction (MI). Because Ang-II plays a central role in post-MI ventricular remodeling, we tested the hypothesis that fibulin-2 modulates Ang-II-induced cardiac remodeling. Methods: Subpressor dosage of Ang-II (0.2 μg/kg/min) was infused over 4 weeks by mini-osmotic-pump in age matched wild-type (WT), heterozygous, and fibulin-2 null (Fbln2 −/− ) adult male mice. Sham mice received normal saline. Results: There was no blood pressure change throughout Ang-II treatment. WT developed significant left ventricular (LV) hypertrophy by Ang-II, whereas Ang-II-treated Fbln2 −/− mice showed no noticeable hypertrophy compared with sham: LV/body weight ratio (WT 4.83±0.18 vs. Fbln2 −/− 4.01± 0.12 mg/g, p < 0.05) and LV posterior wall thickness by echocardiogram (WT 0.76± 0.03 vs. Fbln2 −/− 0.71± 0.02 mm, p < 0.05). Atrial natriuretic peptide (ANP) mRNA expression was significantly increased in Ang-II-treated WT compared with sham, but not in Ang-II-treated Flbn2 −/− . Ang-II also induced significant up-regulation in fibulin-2, Collagen I, Collagen III, and MMP-2 mRNA level in WT, but not in Fbln2 −/− . Both TGF-β1 mRNA and protein expression were significantly up-regulated in Ang-II-treated WT, but were unchanged in Ang-II-treated Fbln2 −/− compared with sham. Activation of TGF-β downstream signaling proteins, phosphorylated forms of Smad2, TGF-β-activated kinase 1 (TAK1), and p38MAPK, were all significantly increased in Ang-II-treated WT, as opposed to no increase in Ang-II-treated Fbln2 −/− compared with sham. Heterozygous mice showed intermediate increase in LV hypertrophy, matrix protein synthesis, and activation of TGF-β downstream signaling pathways between WT and Fbln2 −/− . Conclusions: Our data suggest that fibulin-2 enhances Ang-II-induced myocardial hypertrophy via up-regulation of TGF-β and its downstream signaling pathways in dose-dependent fashion and that fibulin-2 is required for Ang-II-induced TGF-β activation. This research has received full or partial funding support from the American Heart Association, AHA Great Rivers Affiliate (Delaware, Kentucky, Ohio, Pennsylvania & West Virginia).

scholarly journals Baicalein Attenuates Angiotensin II-Induced Cardiac Remodeling via Inhibition of AKT/mTOR, ERK1/2, NF-κB, and Calcineurin Signaling Pathways in Mice

2014 ◽  
Vol 28 (4) ◽  
pp. 518-526 ◽  
Author(s):  
Ai-Wu Wang ◽  
Lina Song ◽  
Jie Miao ◽  
Hong-Xia Wang ◽  
Cui Tian ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Signaling Pathways ◽  
Cardiac Remodeling ◽  
Calcineurin Signaling

Pharmacological blockage of ICAM-1 improves angiotensin II-induced cardiac remodeling by inhibiting adhesion of LFA-1+ monocytes

2019 ◽  
Vol 317 (6) ◽  
pp. H1301-H1311 ◽  
Author(s):  
Qiu-Yue Lin ◽  
Ping-Ping Lang ◽  
Yun-Long Zhang ◽  
Xiao-Lei Yang ◽  
Yun-Long Xia ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cardiovascular Diseases ◽  
Adhesion Molecules ◽  
Vascular Endothelium ◽  
Cardiac Remodeling ◽  
Leukocyte Adhesion ◽  
Neutralizing Antibody ◽  
Ang Ii ◽  
Cardiac Contractile ◽  
And Migration

Intercellular adhesion molecule-1 (ICAM-1) is a member of an immunoglobulin-like superfamily of adhesion molecules that mediate leukocyte adhesion to vascular endothelium and are involved in several cardiovascular diseases, including ischemia-reperfusion injury, myocardial infarction, and atherosclerosis. However, the role of ICAM-1 in angiotensin II (ANG II)-induced cardiac remodeling in mice remains unclear. Wild-type mice were administered an IgG control or ICAM-1 neutralizing antibody (1 and 2 mg/mouse, respectively) and ANG II (1,000 ng·kg−1·min−1) for up to 14 days. Cardiac contractile function and structure were detected by echocardiography. Hypertrophy, fibrosis, and inflammation were assessed by histological examination. The infiltration of lymphocyte function-associated antigen-1 (LFA-1+) monocytes/macrophages was assessed by immunostaining. The mRNA expression of genes was evaluated by quantitative RT-PCR analysis. Protein levels were tested by immunoblotting. We found that ICAM-1 expression in ANG II-infused hearts and ICAM-1 levels in serum from human patients with heart failure were significantly increased. Moreover, ANG II infusion markedly enhanced ANG II-induced hypertension, caused cardiac contractile dysfunction, and promoted cardiac hypertrophy, fibrosis, and LFA-1+ macrophage infiltration. Conversely, blockage of ICAM-1 with a neutralizing antibody dose-dependently attenuated these effects. Moreover, our in vitro data further demonstrated that blocking ICAM-1 inhibited ANG II-induced LFA-1+ macrophage adhesion to endothelial cells and migration. In conclusion, these results provide novel evidence that blocking ICAM-1 exerts a protective effect in ANG II-induced cardiac remodeling at least in part through the modulation of adhesion and infiltration of LFA-1+ macrophages in the heart. Inhibition of ICAM-1 may represent a new therapeutic approach for hypertrophic heart diseases. NEW & NOTEWORTHY Leukocyte adhesion to vascular endothelium is a critical step in cardiovascular diseases. ICAM-1 is a member of immunoglobulin-like superfamily of adhesion molecules that binds LFA-1 to mediate leukocytes adhesion and migration. However, the significance of ICAM-1 in ANG II-induced cardiac remodeling remains unclear. This study reveals that blocking of ICAM-1 prevents ANG II-induced cardiac remodeling via modulating adhesion and migration of LFA-1+ monocytes, may serve as a novel therapeutic target for hypertensive cardiac diseases.

scholarly journals Lutein attenuates angiotensin II- induced cardiac remodeling by inhibiting AP-1/IL-11 signaling

Redox Biology ◽  
2021 ◽  
pp. 102020
Author(s):  
Youming Chen ◽  
Lan Wang ◽  
Shixing Huang ◽  
Jiangfeng Ke ◽  
Qing Wang ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Remodeling

scholarly journals Oxidative Stress as A Mechanism for Functional Alterations in Cardiac Hypertrophy and Heart Failure

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 931
Author(s):  
Anureet K. Shah ◽  
Sukhwinder K. Bhullar ◽  
Vijayan Elimban ◽  
Naranjan S. Dhalla
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Cardiac Remodeling ◽  
Cardiac Dysfunction ◽  
Critical Role ◽  
Pressure Overload ◽  
Hypertrophied Heart ◽  
Vasoactive Hormones

Although heart failure due to a wide variety of pathological stimuli including myocardial infarction, pressure overload and volume overload is associated with cardiac hypertrophy, the exact reasons for the transition of cardiac hypertrophy to heart failure are not well defined. Since circulating levels of several vasoactive hormones including catecholamines, angiotensin II, and endothelins are elevated under pathological conditions, it has been suggested that these vasoactive hormones may be involved in the development of both cardiac hypertrophy and heart failure. At initial stages of pathological stimuli, these hormones induce an increase in ventricular wall tension by acting through their respective receptor-mediated signal transduction systems and result in the development of cardiac hypertrophy. Some oxyradicals formed at initial stages are also involved in the redox-dependent activation of the hypertrophic process but these are rapidly removed by increased content of antioxidants in hypertrophied heart. In fact, cardiac hypertrophy is considered to be an adaptive process as it exhibits either normal or augmented cardiac function for maintaining cardiovascular homeostasis. However, exposure of a hypertrophied heart to elevated levels of circulating hormones due to pathological stimuli over a prolonged period results in cardiac dysfunction and development of heart failure involving a complex set of mechanisms. It has been demonstrated that different cardiovascular abnormalities such as functional hypoxia, metabolic derangements, uncoupling of mitochondrial electron transport, and inflammation produce oxidative stress in the hypertrophied failing hearts. In addition, oxidation of catecholamines by monoamine oxidase as well as NADPH oxidase activation by angiotensin II and endothelin promote the generation of oxidative stress during the prolonged period by these pathological stimuli. It is noteworthy that oxidative stress is known to activate metallomatrix proteases and degrade the extracellular matrix proteins for the induction of cardiac remodeling and heart dysfunction. Furthermore, oxidative stress has been shown to induce subcellular remodeling and Ca2+-handling abnormalities as well as loss of cardiomyocytes due to the development of apoptosis, necrosis, and fibrosis. These observations support the view that a low amount of oxyradical formation for a brief period may activate redox-sensitive mechanisms, which are associated with the development of cardiac hypertrophy. On the other hand, high levels of oxyradicals over a prolonged period may induce oxidative stress and cause Ca2+-handling defects as well as protease activation and thus play a critical role in the development of adverse cardiac remodeling and cardiac dysfunction as well as progression of heart failure.

Zinc finger and BTB domain-containing protein 20 aggravates angiotensin II-induced cardiac remodeling via the EGFR-AKT pathway

2021 ◽  
Author(s):  
Fangfang Li ◽  
Miaomiao Du ◽  
Yiming Yang ◽  
Zhu Wang ◽  
Hu Zhang ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Zinc Finger ◽  
Cardiac Remodeling ◽  
Akt Pathway ◽  
Btb Domain

602 INCREASED CHYMASE DEPENDENT ANGIOTENSIN II-FORMING ACTIVITY IN THE CIRCULATING MONONUCLEAR LEUKOCYTE ASSOCIATED WITH ATRIAL FIBRILLATION AND CARDIAC REMODELING

2012 ◽  
Vol 30 ◽  
pp. e176
Author(s):  
Keisuke Okamura ◽  
Kenzo Matsumoto ◽  
Syunichiro Sumi ◽  
Yosuke Takamiya ◽  
Ken Kitajima ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Angiotensin Ii ◽  
Cardiac Remodeling ◽  
Mononuclear Leukocyte

Ginsenoside Rb1 attenuates angiotensin II-induced abdominal aortic aneurysm through inactivation of the JNK and p38 signaling pathways

2015 ◽  
Vol 73 ◽  
pp. 86-95 ◽  
Author(s):  
Xiao-Jing Zhang ◽  
Chengwei He ◽  
Ke Tian ◽  
Peng Li ◽  
Huanxing Su ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Angiotensin Ii ◽  
Aortic Aneurysm ◽  
Signaling Pathways ◽  
Ginsenoside Rb1 ◽  
Abdominal Aortic

Angiotensin II-Induced Signaling Pathways in Diabetes

2005 ◽  
Vol 1 (2) ◽  
pp. 197-202 ◽  
Author(s):  
Mario Marrero ◽  
David Fulton ◽  
David Stepp ◽  
David Stern
Keyword(s):  
Angiotensin Ii ◽  
Signaling Pathways
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