scholarly journals Carotid arterial mechanics as useful biomarker of extracellular matrix turnover and preserved ejection fraction heart failure

2020 ◽  
Vol 7 (4) ◽  
pp. 1615-1625
Author(s):  
Kevin Ning Zhou ◽  
Kuo‐Tzu Sung ◽  
Chih‐Hsuan Yen ◽  
Cheng‐Huang Su ◽  
Ping‐Ying Lee ◽  
...  
Hypertension ◽  
2013 ◽  
Vol 61 (1) ◽  
pp. 112-119 ◽  
Author(s):  
Dalane W. Kitzman ◽  
David M. Herrington ◽  
Peter H. Brubaker ◽  
J. Brian Moore ◽  
Joel Eggebeen ◽  
...  

2016 ◽  
Vol 252 ◽  
pp. e163
Author(s):  
M. Martínez-Marin ◽  
J. Perez-Calvo ◽  
C. Josa-Laorden ◽  
I. Lacambra-Blasco ◽  
I. Gimenez-Lopez ◽  
...  

2020 ◽  
Vol 21 (18) ◽  
pp. 6742 ◽  
Author(s):  
Merle M. Krebber ◽  
Christian G. M. van Dijk ◽  
Robin W. M. Vernooij ◽  
Maarten M. Brandt ◽  
Craig A. Emter ◽  
...  

Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) are pivotal regulators of extracellular matrix (ECM) composition and could, due to their dynamic activity, function as prognostic tools for fibrosis and cardiac function in left ventricular diastolic dysfunction (LVDD) and heart failure with preserved ejection fraction (HFpEF). We conducted a systematic review on experimental animal models of LVDD and HFpEF published in MEDLINE or Embase. Twenty-three studies were included with a total of 36 comparisons that reported established LVDD, quantification of cardiac fibrosis and cardiac MMP or TIMP expression or activity. LVDD/HFpEF models were divided based on underlying pathology: hemodynamic overload (17 comparisons), metabolic alteration (16 comparisons) or ageing (3 comparisons). Meta-analysis showed that echocardiographic parameters were not consistently altered in LVDD/HFpEF with invasive hemodynamic measurements better representing LVDD. Increased myocardial fibrotic area indicated comparable characteristics between hemodynamic and metabolic models. Regarding MMPs and TIMPs; MMP2 and MMP9 activity and protein and TIMP1 protein levels were mainly enhanced in hemodynamic models. In most cases only mRNA was assessed and there were no correlations between cardiac tissue and plasma levels. Female gender, a known risk factor for LVDD and HFpEF, was underrepresented. Novel studies should detail relevant model characteristics and focus on MMP and TIMP protein expression and activity to identify predictive circulating markers in cardiac ECM remodeling.


2020 ◽  
Vol 21 (17) ◽  
pp. 6013 ◽  
Author(s):  
Camila Hochman-Mendez ◽  
Ernesto Curty ◽  
Doris A. Taylor

No effective medical treatment exists for heart failure with preserved ejection fraction (HFpEF), accounting for approximately half of all heart failure cases. The elevated passive myocardial stiffness in HFpEF is attributed to a combination of alterations in the extracellular matrix (ECM) collagen content and modifications in the sarcomeric protein titin. Here, we propose polylaminin, a biomimetic polymer of laminin, as a promising approach for manipulating the titin isoform shift and phosphorylation in cardiomyocytes. Exploring the pleiotropic effects of polylaminin may be a novel strategy for alleviating symptoms in HFpEF’s multifactorial pathophysiology.


2020 ◽  
Vol 319 (4) ◽  
pp. H765-H774
Author(s):  
Lydia E. Matesic ◽  
Lisa A. Freeburg ◽  
Laura B. Snyder ◽  
Lauren-Ashley Duncan ◽  
Amber Moore ◽  
...  

Heart failure (HF) with a preserved ejection fraction (HFpEF) is a growing cause of HF and commonly afflicts the elderly. Milestones for HFpEF include diastolic dysfunction and an abnormal extracellular matrix (ECM). The ubiquitin ligases, such as WWP1, change with aging and regulate critical protein turnover/stability processes, such as the ECM. The present study demonstrated that induction of WWP1 in mice induced LV hypertrophy, diastolic dysfunction, and ECM accumulation, consistent with the HFpEF phenotype, and thus may identify a new therapeutic pathway.


2008 ◽  
Vol 7 ◽  
pp. 62-63
Author(s):  
J NUNEZ ◽  
L MAINAR ◽  
G MINANA ◽  
R ROBLES ◽  
J SANCHIS ◽  
...  

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