Novel approach yields new molecular insights into cardiac fibrosis
One of the leading causes of all problems that afflict the heart is cardiac fibrosis, which occurs when excess connective tissue starts to form after an injury or stimulus, often becoming a scar. There is perhaps no greater underlying trigger of heart failure.
How fibrosis develops in the heart, at the molecular level, has long been a puzzle that scientists aim to solve. But the difficulty lies in the ability to study actual human tissue samples, which must be collected, processed and stored in careful, specific ways.
An exciting study led by Professor Anthony Gramolini (Department of Physiology/Ted Rogers Centre for Heart Research), Dr. Uros Kuzmanov (Research Associate, Gramolini lab), and Andrew Emili (Director of the Center for Network Systms Bilogy, Boston University) used a unique approach in a new study that leveraged advanced technologies to yield brand new insights into the molecular nature of cardiac fibrosis.
Team members of the study include: Dr. Phyllis Billia (Physiology faculty and Clinician Scientist at UHN), Dr. Sharma Parveen (former Research Associate, Gramolni lab), Julia Kim (MSc graduate, Gramolini lab), Sina Hadipour-Lakmehsari (MSc graduate, Gramolini lab) and Shin-Haw Lee (Physiology PhD student).
“This project not only validates the heart-on-a-chip’s high value in heart disease research, but also delivers new insights into the field, and provides new testable therapeutic approaches, with available compounds,” says Anthony Gramolini. “We are very excited about the potential to exploit these systems, not only for cardiac fibrosis, but also for other cardiomyopathies as well.” This project was funded by the Centre’s Translational Biology and Engineering Program, and by two fellowship awards to researchers in the Gramolini lab.
This project was funded by the Ted Rogers Centre’s Translational Biology and Engineering Program, and by two fellowship awards to researchers in the Gramolini lab.
