Diabetic cardiomyopathy (DiabCM) is common in people with diabetes. It predisposes to heat failure. Its cause remains unclear and there is no specific treatment for DiabCM. Inflammation is a fundamental tissue response to a metabolic insult and it occur in DiabCM. The central hypothesis in this work is that inflammation through myocardial macrophage cells contributes to DiabCM. This hypothesis will be tested in animal models and also in cell culutre studies.
The L-type Calcium Channel As A Reporter Of Successful Morpholino Oligomer Therapy In Treatment Of Duchenne Muscular Dystrophy Cardiomyopathy
Funder
National Health and Medical Research Council
Funding Amount
$595,062.00
Summary
Duchenne Muscular Dystrophy is a fatal muscle wasting disorder. We have previously characterised how the heart fails in a mouse model of muscular dystrophy. We now have preliminary data demonstrating that treatment of mice with morpholino oligomers can rescue cardiac function. This project will fully characterise the effect of the treatment on heart function and optimise therapy regimes with the view to utilising the optimised protocol as a guideline in treating cardiomyopathy in Duchenne Muscul ....Duchenne Muscular Dystrophy is a fatal muscle wasting disorder. We have previously characterised how the heart fails in a mouse model of muscular dystrophy. We now have preliminary data demonstrating that treatment of mice with morpholino oligomers can rescue cardiac function. This project will fully characterise the effect of the treatment on heart function and optimise therapy regimes with the view to utilising the optimised protocol as a guideline in treating cardiomyopathy in Duchenne Muscular Dystrophy boys.Read moreRead less
Cardiomyopathies (heart muscle problems) are the most common inherited heart conditions and represent an important clinical problem. The clinical and psychosocial impact on both the children and their families is significant. The proposed research will improve our understanding of the clinical and genetic basis of childhood cardiomyopathies, and how genetic factors may influence the development, progression, and clinical outcome, including heart failure, transplantation, and sudden death.
Preclinical Relaxin Therapy To Reverse Cardiac Fibrosis And Gain Functional Benefits
Funder
National Health and Medical Research Council
Funding Amount
$724,754.00
Summary
Cardiac fibrosis is a key factor promoting heart disease and onset of complications including arrhythmias and heart failure. There is urgent and unmet need of drugs that can reverse fibrosis. By documenting anti-fibrotic action of a peptide hormone relaxin, CIA and his team will test therapeutic effect of relaxin in heart disease models focusing on fibrosis-reversal and functional gain, particularly arrhythmias. This work would promote development of relaxin as a new cardiovascular drug.
How Does Sudden Cardiac Death Occur In Familial Hypertrophic Cardiomyopathy?
Funder
National Health and Medical Research Council
Funding Amount
$1,312,606.00
Summary
Familial hypertrophic cardiomyopathy is a leading cause of sudden cardiac death but the mechanisms for the induction of arrhythmia are unknown. This proposal has the potential to impact sudden death in the young and enable significant expansion of Australia’s research capacity into the treatment of familial hypertrophic heart disease in humans.
Sudden cardiac death (SCD) is a tragic consequence of a number of heart diseases. The death is often unexpected and has major implications for the family and community. This 3-year study seeks to evaluate clinical, genetic, and long-term outcomes in Australian families where SCD has occurred in a young relative (aged 1-35 years). This study will improve clinical and genetic evaluation of families, resulting in targeted management strategies, with the ultimate goal to prevent SCD.
Innovative Use Of Hydrogel Technology To Recapitulate And Investigate Cardiac Pathology.
Funder
National Health and Medical Research Council
Funding Amount
$716,162.00
Summary
Hypertrophic cardiomyopathy is the leading cause of sudden death in the young. No treatment exists that can reverse or prevent it, primarily because the underlying mechanisms of the disease have not been fully elucidated. I will use innovative hydrogel technology to simulate the disease state. I will use this as a tool to identify the mechanisms involved with development of the disease. This will enable identification of potential therapeutic targets for prevention of the disease.
New CaMKII Therapeutic Targets In Heart Failure With Preserved Ejection Fraction
Funder
National Health and Medical Research Council
Funding Amount
$740,335.00
Summary
Deaths associated with impaired heart muscle relaxation and unstable cardiac cycle rhythm are increasing. The mechanisms by which these pathologies occur are not understood and clinical therapies are lacking. We have novel evidence to suggest that a key signalling protein, CaMKII, is critically involved in the development of these forms of heart pathology. This goal of this project is to identify how CaMKII is implicated in heart failure and dysrhythmia as a basis for designing new therapies.
Diabetic Cardiomyopathy: Defining New Mechanisms Of Cardiomyocyte Injury And Loss
Funder
National Health and Medical Research Council
Funding Amount
$609,320.00
Summary
The heart is recognized as an important casualty organ in the progression of diabetes – both type 1 and type 2. We have new evidence that in diabetic and pre-diabetic hearts there is excess breakdown of heart cell structure in order to scavenge metabolic fuel, and that this scavenging can lead to heart cell death. Our goal is to identify ways in which the heart may be protected against this pathology and to identify new molecular targets for treatment of diabetic hearts.
A Novel Therapy For The Prevention And Treatment Of Familial Hypertrophic Cardiomyopathy
Funder
National Health and Medical Research Council
Funding Amount
$835,972.00
Summary
Familial hypertrophic cardiomyopathy is a genetic disorder that leads to enlargement of the heart, cardiac failure and sudden death. No treatment exists that can reverse or prevent the cardiomyopathy. In this proposal we will determine whether a peptide (Patent WO2013/113060) targeting a calcium channel can prevent or reverse the cardiomyopathy as a novel treatment for the disease.