scholarly journals Pathophysiological Mapping of Experimental Heart Failure: Left and Right Ventricular Remodeling in Transverse Aortic Constriction Is Temporally, Kinetically and Structurally Distinct

2018 ◽  
Vol 9 ◽  
Author(s):  
Mathew J. Platt ◽  
Jason S. Huber ◽  
Nadya Romanova ◽  
Keith R. Brunt ◽  
Jeremy A. Simpson
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Ventricular Remodeling ◽  
Transverse Aortic Constriction ◽  
Aortic Constriction ◽  
Experimental Heart Failure ◽  
Left And Right ◽  
Right Ventricular Remodeling

scholarly journals Right ventricular remodeling and dysfunction among the spectrum of heart failure phenotypes

2016 ◽  
Vol 18 (Suppl 1) ◽  
pp. P73
Author(s):  
Harris Wang ◽  
Lingyu Xu ◽  
Kelvin Chow ◽  
Joseph J Pagano ◽  
Anna Schmidt ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Ventricular Remodeling ◽  
Right Ventricular Remodeling

Abstract 214: Septin4 Deletion Prevents Hypertrophy to Heart Failure Transition After Transverse Aortic Constriction

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Dogacan Yucel ◽  
Jop H Van Berlo ◽  
Preethy Parthiban
Keyword(s):  
Heart Failure ◽  
Ejection Fraction ◽  
Cardiac Function ◽  
Ventricular Remodeling ◽  
Pressure Overload ◽  
Small Gtpase ◽  
Calcium Handling ◽  
Future Research ◽  
Transverse Aortic Constriction ◽  
Aortic Constriction

In response to cardiac injury or increased workload, the mammalian heart undergoes ventricular remodeling to maintain cardiac function. Initally, these changes are compensatory, although ultimately, they can lead to death of cardiomyocytes, ventricular dilation, and progression to heart failure. It is critical to understand the underlying mechanisms that regulate this transition, since it could identify new therapeutic targets. The role of the small GTPase Septin4 in the heart, and in regulating cardiac stress response is unknown. Previous research has implicated Septin 4 in regulation of Store Operated Calcium entry, as well as cell death regulation through a splice isoform (ARTS). We performed cardiac pressure overload in wild type controls and Septin 4 knockout (-/-) mice. Importantly, we did not detect differences in cardiac hypertrophy or function at baseline (57% ejection fraction in both groups). Four weeks following transverse aortic constriction (TAC), Septin4-/- mice showed improved cardiac function with higher ejection fraction (51%) compared to controls (40%), while the level of hypertrophy was similar. Furthermore, we detected reduced cleaved caspase-3 staining after TAC in Septin4-/- mice, due to inhibition of cardiomyocyte apoptosis in Septin4 -/- mice. Mechanistically, we detected increases in protein expression of both total and phosphorylated phospholamban and CaMKII in Septin4-/- mice, suggesting alterations in Calcium handling, and indicating compensatory signaling pathways were still active in Septin4-/- mice, while control mice were transitioning to heart failure. In conclusion, genetic deletion of Septin4 prevented cardiomyocyte death and protected mice from heart failure following cardiac pressure overload. Future research will focus on regulation of calcium handling in Septin4-/- mice to determine the exact mechanisms through which Septin4 plays a detrimental role in cardiac remodeling.

Wnt Signaling Pathway in Right Ventricular Remodeling

Pneumologie ◽  
2012 ◽  
Vol 66 (06) ◽  
Author(s):  
A Tretyn ◽  
KD Schlüter ◽  
W Janssen ◽  
HA Ghofrani ◽  
F Grimminger ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Wnt Signaling ◽  
Signaling Pathway ◽  
Ventricular Remodeling ◽  
Wnt Signaling Pathway ◽  
Right Ventricular Remodeling
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