Improving outcomes for people with heart disease
Dr Adam Trewin is working to better understand the cause of damage to the heart muscle cells due to ischemia – the lack of oxygen and nutrients – that occurs during a heart attack.
Through research funded by a Cardiac Society of Australia and New Zealand (CSANZ) Bayer Young Investigator Research Grant, Dr Trewin is investigating the underlying molecular mechanisms that regulate the ‘energy powerhouses’ of heart muscle cells known as mitochondria.
Mitochondria are essential for a range of critical cellular processes, yet they are extremely sensitive to ischemic injury. Damage to mitochondria is a key driver of the outcome of ischemic heart disease, which is the leading cause of death in Australia.
‘If ischemia occurs for a prolonged period, the damaged mitochondria release ‘self-destruct’ signals which drives irreversible cell death processes and heart muscle injury,’ Dr Trewin explained.
Specifically, the aim of this project is to determine whether specific types of genes known as ‘long non-coding RNA’ can regulate mitochondrial function to protect them from damage during ischemia in order to mitigate subsequent heart muscle cell death.
Identifying new long non-coding RNAs that regulate mitochondrial function in response to ischemia may reveal potential therapeutic targets. This means that new treatments could be developed to act on a non-coding RNA in order to reduce the severity of injury or improve functional recovery of the heart.
As part of his laboratory studies, Dr Trewin will use cells grown from heart tissue and conduct experiments using these cells to simulate ischemia in the heart.
‘To identify candidate long non-coding RNAs from these heart cell experiments, we will conduct RNA-sequencing analyses. The most promising ones will then be studied with additional experiments in heart cells to better understand their role in regulating mitochondrial function,’ Dr Trewin explained.
‘This basic research is a vital first step towards opening new avenues of investigation that could ultimately lead to drug development and clinical translation.’