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Oxidative stress and inflammation are now recognised as important causal factors of diabetic cardiac and vascular injury. Building on evidence generated in our laboratory, we have identified that lowering oxidative stress by targeting a major regulator of oxidative stress, namely the transcription factor Nrf2, additionally lessens inflammation and importantly, reduces vascular disease in diabetic mice.

Our preliminary in vitro evidence in bone marrow derived macrophages (BMDMs) suggests that Nrf2 activation lessens the priming of a key component of the inflammatory machinery, namely the NLRP3 inflammasome. This is a critical initial step in the activation of the NLRP3-inflammasome, and the demonstration that Nrf2 activation is able to limit this step, holds promise for interventions to limit inflammatory driven disease. Importantly, the exact mechanism as to how this is occurring is currently unknown. This project builds on these exciting findings by further exploring the key mechanisms, as well as determining the contribution of key components of both arms of the axis, to the anti-inflammatory action of the Nrf2 activators.


  1. To investigate whether Nrf2 activation protects against cardiac complications of type 2 diabetes.
  2. To investigate whether pharmacological and genetic inhibition of the NLRP3 inflammasome protects against type 2 diabetes-mediated vascular and cardiac injury.
  3. To investigate whether dual targeting of the axis (Nrf2 activation and NLRP3 inhibition) further augments inhibition of diabetic vascular and cardiac complications.
  4. To elucidate the mechanisms whereby upregulation of Nrf2 lessens NLRP3 activation in activated diabetic macrophages.

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