scholarly journals Differential expression of Gs in a murine model of homocysteinemic heart failure

2008 ◽  
pp. 79 ◽  
Author(s):  
Thomas Vacek
Keyword(s):  
Heart Failure ◽  
Differential Expression ◽  
Murine Model

Abstract P394: Angiotensin-(1-7) Attenuates Diastolic Dysfunction And Cardiac Remodeling In Murine Model Of Heart Failure With Preserved Ejection Fraction

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Pariya Edalat ◽  
Karina Gomes ◽  
Noura N Ballasy ◽  
Anshul S Jadli ◽  
Darrell D Belke ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Cardiac Hypertrophy ◽  
Diastolic Dysfunction ◽  
Murine Model ◽  
Cardiac Remodeling ◽  
Control Group ◽  
Chow Diet ◽  
Preserved Ejection Fraction ◽  
Phosphorylation Level

Background: Heart failure with preserved ejection fraction (HFpEF) is a global public health epidemic that accounts for half of the heart failure cases. Various therapeutic approaches have been tested to block the activation of the Renin-Angiotensin System (RAS), including AT1R blockers (ARBs), Angiotensin-Converting Enzyme (ACE) inhibitors (ACEi), and direct renin inhibitors (DRIs) with modest to negligible benefits. The discovery of ACE2, a novel homolog of ACE, has advanced our understanding of the RAS. ACE2 is a monocarboxypeptidase that degrades Ang II into Ang-(1-7), which works via the activation of the Mas receptor. It has been well understood that the actions of Ang-(1-7) attenuate cardiac remodeling, production of ROS, and cardiac fibrosis. Objective: To determine the therapeutic role of Ang-(1-7) in HFpEF and identify the molecular mechanism related to its action. Methods and Results: To generate a murine model of HFpEF, male WT mice (n=24) were subjected to HFD in addition to eNOS inhibition with L-NAME (0.5 g l-1 in drinking water), as previously described. The control group (n=12) received chow diet and normal tap water. The murine model of HFpEF was validated using the non-invasive transthoracic echocardiography and invasive pressure-volume (PV) loop analyses, which exhibited diastolic dysfunction as well as cardiac hypertrophy. To evaluate the effects of Ang-(1-7) on HFpEF, animals were administered with either saline (n=12) or Ang-(1-7) (n=12) (24 μg/kg/day) for four weeks. Ang-(1-7) treatment improved diastolic function by reducing LVEDP (Ctrl: 8.267±1.254; HFD+L-NAME: 17.64±1.925; Ang-(1-7): 9.100±1.578) and Tau value (Ctrl: 7.365±0.5752; HFD+L-NAME: 9.224±0.3569; Ang-(1-7): 7.381±0.3041). Furthermore, Ang-(1-7) reduced cardiac hypertrophy by reducing the phosphorylation level of MAPK ERK 1/2 (Ctrl: 0.9074±0.1088; HFD+L-NAME: 1.212±0.1369; Ang-(1-7): 0.5615±0.1502) and increasing the phosphorylation level of AMPK (Ctrl: 0.1502±0.1502; HFD+L-NAME: 0.6127±0.06414; Ang-(1-7): 0.7852±0.1006). Ang-(1-7) treatment also reduces cardiomyocytes’ size and decreases interstitial fibrosis, as indicated by WGA and PSR staining. Conclusion: Ang-(1-7) treatment attenuated the development of HFD+L-NAME-induced HFpEF, reduced cardiac hypertrophy, and improved metabolic function.

scholarly journals MYOSTATIN INHIBITION IMPROVES CARDIAC GLUCOSE METABOLISM IN A MURINE MODEL OF HEART FAILURE

2015 ◽  
Vol 65 (10) ◽  
pp. A1626
Author(s):  
Estibaliz Castillero ◽  
Hirokazu Akashi ◽  
Ruiping Ji ◽  
Catherine Wang ◽  
Ziad Ali ◽  
...  
Keyword(s):  
Heart Failure ◽  
Glucose Metabolism ◽  
Murine Model ◽  
Myostatin Inhibition

scholarly journals Development of a murine model of heart failure with preserved ejection fraction

2018 ◽  
Vol 10 (2) ◽  
pp. 198
Author(s):  
J. Imbault ◽  
A. Abelanet ◽  
E.F. Damar Ali ◽  
E. Roux ◽  
A. Ouattara ◽  
...  
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Murine Model ◽  
Preserved Ejection Fraction

Induction of a Pro-Inflammatory State by Hemodynamic Load in a Murine Model of Heart Failure

2007 ◽  
Vol 13 (6) ◽  
pp. S92-S93
Author(s):  
Keith Youker ◽  
Lindsey Rudloff ◽  
Christian Assad-Kottner ◽  
Guillermo Torre-Amione
Keyword(s):  
Heart Failure ◽  
Murine Model ◽  
Inflammatory State
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