Heart Plasticity in Response to Pressure- and Volume-Overload: A Review of Findings in Compensated and Decompensated Phenotypes

Pitoulis, Fotios G.; Terracciano, Cesare M.

doi:10.3389/fphys.2020.00092

Cited by 50 publications

(49 citation statements)

References 161 publications

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“…This will induce reactive fibrosis and LV hypertrophy in an effort to maintain cardiac output. Eventually, this will fail and cause a decline in cardiac pump function (Pitoulis and Terracciano, 2020).…”

Section: Discussionmentioning

confidence: 99%

Defective Autophagy in Vascular Smooth Muscle Cells Alters Vascular Reactivity of the Mouse Femoral Artery

et al. 2020

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Autophagy is an important cellular survival process that enables degradation and recycling of defective organelles and proteins to maintain cellular homeostasis. Hence, defective autophagy plays a role in many age-associated diseases, such as atherosclerosis, arterial stiffening and hypertension. Recently, we showed in mice that autophagy in vascular smooth muscle cells (VSMCs) of large elastic arteries such as the aorta is important for Ca 2+ mobilization and vascular reactivity. Whether autophagy plays a role in the smaller muscular arteries, such as the femoral artery, and thereby contributes to for example, blood pressure regulation is currently unknown. Therefore, we determined vascular reactivity of femoral artery segments of mice containing a VSMC specific deletion of the essential autophagy gene Atg7 (Atg7 F/F SM22α-Cre +) and compared them to femoral artery segments of corresponding control mice (Atg7 +/+ SM22α-Cre +). Our results indicate that similar to the aorta, femoral artery segments showed enhanced contractility. Specifically, femoral artery segments of Atg7 F/F SM22α-Cre + mice showed an increase in phasic phenylephrine (PE) induced contractions, together with an enhanced sensitivity to depolarization induced contractions. In addition, and importantly, VSMC sensitivity to exogenous nitric oxide (NO) was significantly increased in femoral artery segments of Atg7 F/F SM22α-Cre + mice. Notwithstanding the fact that small artery contractility is a significant pathophysiological determinant for the development of hypertension, 7 days of treatment with angiotensin II (AngII), which increased systolic blood pressure in control mice, was ineffective in Atg7 F/F SM22α-Cre + mice. It is likely that this was due to the increased sensitivity of VSMCs to NO in the femoral artery, although changes in the heart upon AngII treatment were also present, which could also be (partially) accountable for the lack of an AngII-induced rise in blood pressure in Atg7 F/F SM22α-Cre + mice. Overall, our study indicates that apart from previously shown effects on large elastic arteries, VSMC autophagy also plays a pivotal role in the regulation of the contractile and relaxing properties of the smaller muscular arteries. This may suggest a role for autophagy in vascular pathologies, such as hypertension and arterial stiffness.

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Section: Discussionmentioning

confidence: 99%

Defective Autophagy in Vascular Smooth Muscle Cells Alters Vascular Reactivity of the Mouse Femoral Artery

et al. 2020

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“…Contraction is the primary function of the myocardium. Cardiac remodeling and changes in mechanical load affect contractile function, with corresponding changes at the structural and molecular level [ 37 ]. Contractile function measurements are typically performed in an organ bath employing an isometric force transducer.…”

Section: Contractile Functionmentioning

confidence: 99%

A practical guide for investigating cardiac physiology using living myocardial slices

Watson

Dendorfer²,

Thum

et al. 2020

Basic Res Cardiol

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Ex vivo multicellular preparations are essential tools to study tissue physiology. Among them, the recent methodological and technological developments in living myocardial slices (LMS) are attracting increasing interest by the cardiac research field. Despite this, this research model remains poorly perceived and utilized by most research laboratories. Here, we provide a practical guide on how to use LMS to interrogate multiple aspects of cardiac function, structure and biochemistry. We discuss issues that should be considered to conduct successful experiments, including experimental design, sample preparation, data collection and analysis. We describe how laboratory setups can be adapted to accommodate and interrogate this multicellular research model. These adaptations can often be achieved at a reasonable cost with off-the-shelf components and operated reliably using well-established protocols and freely available software, which is essential to broaden the utilization of this method. We will also highlight how current measurements can be improved to further enhance data quality and reliability to ensure inter-laboratory reproducibility. Finally, we summarize the most promising biomedical applications and envision how living myocardial slices can lead to further breakthroughs.

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“…Cardiac plasticity permits the heart to adjust its function and structure in response to environmental stimuli such as the increase in the wall thickness or the dilatation of the ventricles due to pressure or volume overload conditions [1]. The term cardiomyopathy (CM) is used to describe an inhomogeneous group of disorders affecting the function and the structure of the myocardial wall without an obvious triggering factor such as arterial hypertension, coronary artery disease, valvular disease or congenital heart disease.…”

Section: Introductionmentioning

confidence: 99%

Updating the Risk Stratification for Sudden Cardiac Death in Cardiomyopathies: The Evolving Role of Cardiac Magnetic Resonance Imaging. An Approach for the Electrophysiologist

et al. 2020

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The prevention of sudden cardiac death (SCD) in cardiomyopathies (CM) remains a challenge. The current guidelines still favor the implantation of devices for the primary prevention of SCD only in patients with severely reduced left ventricular ejection fraction (LVEF) and heart failure (HF) symptoms. The implantation of an implantable cardioverter-defibrillator (ICD) is a protective barrier against arrhythmic events in CMs, but the benefit does not outweigh the cost in low risk patients. The identification of high risk patients is the key to an individualized prevention strategy. Cardiac magnetic resonance (CMR) provides reliable and reproducible information about biventricular function and tissue characterization. Furthermore, late gadolinium enhancement (LGE) quantification and pattern of distribution, as well as abnormal T1 mapping and extracellular volume (ECV), representing indices of diffuse fibrosis, can enhance our ability to detect high risk patients. CMR can also complement electro-anatomical mapping (EAM), a technique already applied in the risk evaluation and in the ventricular arrhythmias ablation therapy of CM patients, providing a more accurate assessment of fibrosis and arrhythmic corridors. As a result, CMR provides a new insight into the pathological substrate of CM. CMR may help identify high risk CM patients and, combined with EAM, can provide an integrated evaluation of scar and arrhythmic corridors in the ablative therapy of ventricular arrhythmias.

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Heart Plasticity in Response to Pressure- and Volume-Overload: A Review of Findings in Compensated and Decompensated Phenotypes

Cited by 50 publications

References 161 publications

Defective Autophagy in Vascular Smooth Muscle Cells Alters Vascular Reactivity of the Mouse Femoral Artery

Defective Autophagy in Vascular Smooth Muscle Cells Alters Vascular Reactivity of the Mouse Femoral Artery

A practical guide for investigating cardiac physiology using living myocardial slices

Updating the Risk Stratification for Sudden Cardiac Death in Cardiomyopathies: The Evolving Role of Cardiac Magnetic Resonance Imaging. An Approach for the Electrophysiologist

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