Unravelling the energy supply and demand pathway in broken heart syndrome

The heart continuously adapts to the body’s changing demands, whether we eat, sleep, work, or exercise, while maintaining metabolic energy balance. Cardiac contraction is a highly energy-demanding process, with most ATP produced by mitochondrial aerobic metabolism. Under stress, surges in stress hormones accelerate heart rate and workload, prompting mitochondria to increase energy supply. However, prolonged or extreme stress can disrupt this balance, causing bioenergetic mismatch and contributing to non-ischemic heart attack, cardiomyopathy, arrhythmias, or heart failure. The mechanisms driving this breakdown remain poorly understood.

This project will investigate how bioenergetic pathways become dysregulated during sustained stress. Using a pharmacological challenge to induce stress cardiomyopathy in rats, we will examine the interplay between stress, excitation–contraction coupling, and mitochondrial function. By integrating structural, functional, and computational analyses across multiple scales, we aim to provide new insights into how the heart fails to cope with stress. This is a vital fundamental step to developing a remediation strategy for stress-induced heart diseases.

• Bachelor’s or master’s degree in bioengineering or biomedical sciences
• Experimental physiology would be desirable

This project is eligible for funding but is subject to eligibility criteria & funding availability.

Page expires: 28 February 2026