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Regulation Of Heart Development And Regeneration By DNA Methylation.
Funder
National Health and Medical Research Council
Funding Amount
$552,709.00
Summary
The adult mammalian heart has an extremely limited capacity for regeneration following a heart attack, which is in stark contrast to the robust regenerative capacity of the newborn heart. How and why mammals lose their ability to regenerate heart tissue after birth is not well understood. We propose a new approach to unravel the complex mechanisms that control gene expression during heart development in rodents and humans, which could provide new therapeutic avenues for heart regeneration.
Regulation Of Endogenous Heart Regeneration By An Anti-fibrotic MicroRNA.
Funder
National Health and Medical Research Council
Funding Amount
$440,949.00
Summary
In contrast to the adult heart, the newborn heart undergoes scarless healing following a heart attack. The molecular mechanisms that govern heart regeneration in newborn mammals are not fully understood. The goal of the current study is to determine the role of a recently identified family of molecules known as microRNAs in the regulation of scarless healing. We propose a novel strategy for re-activation of microRNAs in the adult heart to promote regeneration following heart attack.
Annexin-A1 Agonists Rescue Cardiac Contractile Function After Myocardial Infarction
Funder
National Health and Medical Research Council
Funding Amount
$621,419.00
Summary
Myocardial infarction (or heart attack, a result of reduced coronary blood flow) and subsequent heart failure are the major cause of death in Western societies; this is expanding to all corners of the globe. New treatments for heart attack are thus essential. We have discovered that the natural hormone annexin-A1 rescues heart muscle function over the short-term, and propose that drugs based on annexin-A1 will prevent cardiac dysfunction of heart muscle up to several weeks after heart attack.
Cytoprotective And Metabolic Responses To Biased Agonists Acting At Cardiomyocyte Gq-coupled Receptors
Funder
National Health and Medical Research Council
Funding Amount
$723,742.00
Summary
Cell surface receptors mediate the response of cardiac muscle cells to hormones and transmitters by interacting with a repertoire of intracellular signalling proteins. Despite primary coupling to Gq proteins that activate shared pathways, four such receptors promote differing responses in cardiac cells. We will investigate signalling pathways differentially activated by the ?1A-adrenergic receptor that promote survival of cardiac muscle under conditions of cell damage or nutrient insufficiency.
Obstructive sleep apnea (OSA) affects 7% of the population and is increasing with the global epidemic of obesity. Research suggests that OSA may be a cause of premature cardiovascular (CV) disease, but definitive proof is lacking. This 5-year trial will answer this question by comparing the rate of CV events (eg stroke, heart attack) in OSA patients who are treated, versus those not treated, with CPAP. The results may lead to a new medical approach to the prevention of CV disease.
The Sleep Apnea Cardio Vascular Endpoints (SAVE) Study
Funder
National Health and Medical Research Council
Funding Amount
$1,177,047.00
Summary
Obstructive sleep apnea (OSA) affects 7% of the population and is increasing with the global epidemic of obesity. Research suggests that OSA may be a cause of premature cardiovascular (CV) disease, but definitive proof is lacking. This 5-year trial will answer this question by comparing the rate of CV events (eg stroke, heart attack) in OSA patients who are treated, versus those not treated, with CPAP. The results may lead to a new medical approach to the prevention of CV disease.
Genome-wide Analysis Of Gene Regulatory Networks In Heart Development And Congenital Heart Disease
Funder
National Health and Medical Research Council
Funding Amount
$1,263,954.00
Summary
Despite advances in surgical methods and hospital critical care, congenital heart disease (CHD) remains the leading cause of non-infectious death in children in the first year of life. Severe CHD requires multiple surgeries and a lifetime of emotional and financial burden. In this proposal we will use new molecular and genetic approaches to ask how the network of genes that normally participates in heart development is controlled by regulatory factors, and how the network is disturbed in CHD.
Targeting Necroptosis Signalling To Counter Stroke-induced Brain Injury
Funder
National Health and Medical Research Council
Funding Amount
$605,809.00
Summary
The origins of the brain injury that arises from stroke remain a matter of enormous interest. Our work suggests that a poorly understood form of cell death, termed necroptosis, contributes to injury to the brain following stroke. In addition to developing an advanced understanding of this process, we will use drugs developed at the Walter and Eliza Hall Institute to test whether blocking this process might be a plausible therapeutic strategy in stroke patients.
Tenecteplase Versus Alteplase For Stroke Thrombolysis Evaluation (TASTE) Trial
Funder
National Health and Medical Research Council
Funding Amount
$4,180,030.00
Summary
Tenecteplase versus Alteplase for Stroke Thrombolysis Evaluation (TASTE) is an Australian-led international randomised trial designed to generate practice-changing evidence by translating the advanced imaging treatment selection approach used in our previous pilot studies. TASTE aims to confirm the superiority of the new-generation clot-dissolving agent, tenecteplase, over the standard agent, alteplase, in the broad group of stroke patients eligible for acute clot-dissolving treatment.
Probing The Cardiac Gene Regulatory Network In Development And Congenital Heart Disease
Funder
National Health and Medical Research Council
Funding Amount
$518,118.00
Summary
In Australia, congenital heart disease (CHD) is the biggest killer of children under 5 years. Defects range from small holes to severe malformations requiring multiple surgeries and an uncertain future. Our appreciation of CHD mechanism is limited. Using cutting-edge technologies in genomics, biophysics and structural biology, we will study the mechanisms that lead to CHD at unprecedented resolution. Our project will progress the concept of personalized diagnosis and treatment of CHD.