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Condition: Cardiomyopathy
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Total 7 results found since Jan 2013.

Impaired Activity of Ryanodine Receptors Contributes to Calcium Mishandling in Cardiomyocytes of Metabolic Syndrome Rats
Conclusion Principal findings of this work are that abnormal Ca2+ transient amplitude, contractile dysfunction; and impaired relaxation of MetS cardiomyocytes underlies intrinsic dysfunctional RyR2 and SERCA pump. Abnormal activity of RyRs was evidenced by its decreased ability to bind [3H]-ryanodine. Although the MetS condition does not modify RyR2 protein expression, its phosphorylation at Ser2814 is decreased, which impairs its capacity for activation during ECC. The dysfunctional RyRs, together with a decreased activity of SERCA pump due to decreased Thr17-PLN phosphorylation suggest a downregulation of CaMKII in MetS...
Source: Frontiers in Physiology - April 29, 2019 Category: Physiology Source Type: research

Age-Dependence of Flow Homeostasis in the Left Ventricle
Conclusions: In average, blood spends 1 to 3 beats inside the LV with very low shear stress rates. The apical region is the most prone to blood stasis, particularly in mid-aged adults. The washout of blood in the normal LV is age-dependent due to physiological changes in the degree of apical penetration of the filling waves. Introduction Cardioembolic stroke is a major source of mortality and disability worldwide and blood stasis one of its major determinants (Adams et al., 1986). Left ventricular (LV) function has evolved to maximize mechanical efficiency and ensure organ perfusion at a low cost of energy and fill...
Source: Frontiers in Physiology - April 25, 2019 Category: Physiology Source Type: research

Atrial Transcriptional Profiles of Molecular Targets Mediating Electrophysiological Function in Aging and Pgc-1 β Deficient Murine Hearts
Conclusion: These findings limit the possible roles of gene transcriptional changes in previously reported age-dependent pro-arrhythmic electrophysiologial changes observed in Pgc-1β-/- atria to an altered Ca2+-ATPase (Atp2a2) expression. This directly parallels previously reported arrhythmic mechanism associated with p21-activated kinase type 1 deficiency. This could add to contributions from the direct physiological outcomes of mitochondrial dysfunction, whether through reactive oxygen species (ROS) production or altered Ca2+ homeostasis. Introduction Atrial arrhythmias constitute a major public health pro...
Source: Frontiers in Physiology - April 23, 2019 Category: Physiology Source Type: research

A Chinese Family With Adult-Onset Leigh-Like Syndrome Caused by the Heteroplasmic m.10191T > C Mutation in the Mitochondrial MTND3 Gene
Conclusion The m.10191T>C mutation in the mtDNA of the complex I (CI) subunit of MTND3 results in the substitution of a highly conserved amino acid (p.Ser45Pro) within the ND3 protein, leading to CI dysfunction through impaired enzyme catalysis rather than impaired stability or assembly, causing a broad clinical spectrum of disorders (26). Patients with the m.10191T>C mutation are rare. In the present study, we report on a family of patients with the extremely rare adult-onset Leigh-like syndrome with the m.10191T>C mutation. Including the two patients from our reported family, the m.10191T...
Source: Frontiers in Neurology - April 17, 2019 Category: Neurology Source Type: research

Nrf2 as a Potential Mediator of Cardiovascular Risk in Metabolic Diseases
Conclusion Activation of the Nrf2-dependent antioxidant system plays an important role in cell defense against oxidative stress damage, whereas the insufficiency of the Nrf2 system is associated with multiple aspects of the genesis and progression of metabolic diseases, posing a great risk to the cardiovascular system (Figure 1). The systemic increase of Nrf2 activity by several activators may be beneficial in the treatment of metabolic diseases. In addition, selective upregulation of Nrf2 genes may represent a potential therapy in obesity, diabetes and atherosclerosis. Looking to the future, experimental research that el...
Source: Frontiers in Pharmacology - April 11, 2019 Category: Drugs & Pharmacology Source Type: research

'Exercise pill' could potentially help people with heart failure
Conclusion The protein hCT1 caused heart muscles to grow in a more healthy way in rodents with heart failure. When treatment stopped, the heart went back to its original condition – something that does not happen when the heart grows in a dysfunctional way. There is currently no cure for heart failure and treatment is only available for keeping symptoms under control. Therefore, this very promising early-stage research with potential for developing a drug for people with heart failure, has huge implications. However, it is important to remember that as this is experimental laboratory research, there are many more stage...
Source: NHS News Feed - August 9, 2017 Category: Consumer Health News Tags: Heart/lungs Source Type: news

CardioPulse Articles * The European Society of Cardiology in Arabia * Health in the Arab world * Guidelines for a successful European Society of Cardiology grant application * Tako-Tsubo cardiomyopathy * Does aetiology matter in secondary prevention of stroke?
Source: European Heart Journal - May 14, 2014 Category: Cardiology Tags: CardioPulse Source Type: research