Unraveling Fibrosis By Pharmacological Targeting Of The G Protein-coupled Receptor, RXFP1
Funder
National Health and Medical Research Council
Funding Amount
$798,618.00
Summary
Peptides, with their high specificity and low toxicity profiles, are highly attractive alternatives to small molecule drugs. H2 relaxin, a peptide hormone, has a strong potential for treating fibrosis. However, the large size of H2 relaxin makes it difficult and expensive to manufacture. Once administered to patients, it is also quickly degraded. We have developed a small anti-fibrotic relaxin peptide, and propose to understand its mechanism of action and improve its therapeutic indices.
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.
This project will substantially improve our understanding of the potential causes of vascular complications of pregnancy including preeclampsia, and provide a solid foundation to develop new clinical interventions for women who develop this disease during their pregnancy. It will also investigate if a peptide hormone, relaxin, could be an effective treatment to manage the health of women diagnosed with preeclampsia during their pregnancy and prevent delivery of severely premature infants.
This fellowship support will allow A/Prof Xiao-Jun DU to pursue his recent pre-clinical research findings on novel therapeutic interventions for cardiovascular diseases. He will particularly focus on new treatment of accumulation of excessive scar tissues (fibrosis) in the heart and large arteries following disease and cardiac inflammation, factors knowing to play pivotal roles in progression of cardiovascular diseases.