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The L-type Calcium Channel In Cardiovascular Health And Disease
Funder
National Health and Medical Research Council
Funding Amount
$631,370.00
Summary
Calcium influx into cardiac muscle cells occurs via the L-type calcium channel. The channel is essential to life but when function is altered it can contribute to the development of sudden death and heart failure. I have made significant discoveries in understanding the role of the channel in disease and I have exploited this knowledge to design therapy including a novel class of calcium channel antagonists to prevent the development of heart failure.
Cellular Metabolism And Signalling In Cardiac Development And Congenital Disease
Funder
National Health and Medical Research Council
Funding Amount
$151,061.00
Summary
This project aims to investigate how the paediatric heart responds to oxidative cellular stresses during cardiac development, surgical stress and congenital heart disease. Pre-surgical interventions aims at improving cardiac function following surgery will be examined, with cellular models being used to determine molecular pathways of cardioprotection, as well as testing agents which may limit cellular damage under surgical stress and disease.
Characterising The Effects Of Oxidative Stress On The Human L-type Ca2+ Channel Isoforms And Role In Human Pathology
Funder
National Health and Medical Research Council
Funding Amount
$250,805.00
Summary
Oxidative stress, poor energy production and increases in intracellular calcium are features of the failing heart. I have determined that the function of the L-type calcium channel, the primary protein responsible for calcium influx and contraction can be regulated by free radicals produced by the mitochondria (powerhouse of the cell). This proposal will determine the site of modification on the human L-type calcium channel and how communication between the channel and the mitochondria is altere ....Oxidative stress, poor energy production and increases in intracellular calcium are features of the failing heart. I have determined that the function of the L-type calcium channel, the primary protein responsible for calcium influx and contraction can be regulated by free radicals produced by the mitochondria (powerhouse of the cell). This proposal will determine the site of modification on the human L-type calcium channel and how communication between the channel and the mitochondria is altered in animal models of human disease.Read moreRead less
The Role Of Aquaporins In Cardiac Ischaemia And Reperfusion
Funder
National Health and Medical Research Council
Funding Amount
$412,670.00
Summary
We are studying the important clinical problem of why the heart doesn't work very well after it has been deprived of blood. This may occur during a heart attack due to coronary artery disease and during cardiac surgery when the heart is stopped. The problem affects children as well as adults undergoing surgery. The reason the heart doesn't work well is related to energy supply and tissue damage caused during the shortage of blood supply and the period soon after flow is restored. Until the heart ....We are studying the important clinical problem of why the heart doesn't work very well after it has been deprived of blood. This may occur during a heart attack due to coronary artery disease and during cardiac surgery when the heart is stopped. The problem affects children as well as adults undergoing surgery. The reason the heart doesn't work well is related to energy supply and tissue damage caused during the shortage of blood supply and the period soon after flow is restored. Until the heart recovers, inadequate pump function may cause low blood flow problems downstream in vital organs such as the brain and kidneys. Under the microscope, a common feature of affected hearts is swelling of the cells and of the energy producing parts called mitochondria. We have identified, for the first time, unique proteins that allow water to move into and around cells of the heart. These proteins are called 'aquaporins' and early results suggest they are involved in how mitochondria deal with a shortage of blood supply. Interestingly, aquaporins are also affected in diseases that affect muscle strength, and we are using what is known in these diseases to further study the role of aquaporins in the heart. Our experiments to will test heart function from the level of the cell, all the way up to the whole heart. To improve the power of our experiments, we are working with mice that lack the special water transport proteins, as a prelude to developing drug therapy for this important problem. By manipulating aquaporin levels or function, we plan to improve heart preservation during periods of no blood flow, and after surgery. This would importantly reduce the risks associated with heart attack and cardiac surgery by avoiding complications associated with poor pump function.Read moreRead less