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Heart disease

We are developing new anti-inflammatory therapies that prevent the development of atherosclerotic lesions, which can rupture and stop blood from getting to the heart, causing a heart attack. We are also asking whether these anti-inflammatory therapies can heal the tissue damage that is caused by a heart attack.

In particular, we are complexing a new class of nanoparticles with clinically viable peptides and small molecule drugs that inhibit inflammation and oxidative stress in the heart and blood vessels. We envisage that these new nanotherapeutics will reduce the risk of having a heart attack and prevent tissue damage if a heart attack does occur. The research uses biochemical and molecular biology techniques as well as novel pre-clinical models of cardiovascular disease as well as the very aggressive form of heart disease that occurs in people with diabetes. The work crosses the disciplines of pharmacology and vascular biology.

We are also studying the molecular mechanisms by which vascular endothelial cells transform into pro-inflammatory mesenchymal-like cells via the process of endothelial-to-mesenchymal (EndMT). EndMT promotes the development of rupture-prone atherosclerotic lesions and we have identified new molecular signaling events driving this process that will inform the discovery of new treatments for inhibiting EndMT in cardiovascular disease. This project involves biochemistry, as well as cell and molecular biology.

Type 1 diabetes

Type 1 diabetes is an autoimmune disease in which insulin-producing cells in the pancreas are destroyed by activated T-cells and glucose can no longer be removed from blood. There is no cure for this disease, with the only treatment being regulation of blood glucose levels by multiple insulin injections every day. However, these injections can reduce blood glucose levels to an extent that is potentially lethal. Moreover, they treat the symptoms, not the underlying cause of the disease.

We have identified a peptide with the capacity to regenerate new insulin-producing cells in the pancreas and stop T-cell expansion, thus decreasing, and possibly removing, the dependence of patients with type 1 diabetes on insulin injections. Further development of this project towards clinical translation using gold-standard pre-clinical models of type 1 diabetes involves multiple skill sets including molecular biology, cell biology and pharmacology. We are also developing strategies for preparing peptides that can be taken by mouth and delivered specifically to the pancreas.