Researchers at the University of Bologna have uncovered a link between glucocorticoid hormones and the heart’s limited ability to repair itself after a heart attack. Their work also points toward a method to restore regenerative potential in heart tissue. The findings appeared in Nature Cardiovascular Research and open doors to new approaches for treating patients who have suffered a heart attack.
In their experiments, the team detected several glucocorticoid receptors scattered throughout the heart tissue of newborn mice. By disabling the activity of these receptors through genetic modification, they observed a striking pause in the maturation of heart cells. Instead of exiting the cell cycle and maturing, the heart cells kept dividing and growing, effectively delaying differentiation when the receptor function was blocked.
The researchers then tested a glucocorticoid receptor blocker that is already approved for human use. The blocker produced the same effect on heart cell behavior, reinforcing the idea that manipulating glucocorticoid signaling could influence cardiac regeneration. The team now plans to explore additional stimuli that promote heart repair, aiming to translate these insights into therapies for heart attack patients.
It is well established that heart tissue does not regenerate robustly after injury. In early life, heart muscle cells reduce their proliferative capacity and increase in size rather than dividing to replace damaged tissue. The study’s authors also demonstrated that glucocorticoids, hormones essential for fetal lung maturation, play a pivotal role in driving this transition away from cell division. Modulating this hormonal pathway could therefore unlock a regenerative window in the heart that is typically closed after birth.
The international collaboration involved researchers from the Weizmann Institute of Science in Rehovot, the Institute of Biochemistry and Cell Biology of the Italian National Research Council, King’s College London, and Sapienza University of Rome. The cross-disciplinary effort combined developmental biology, cardiology, and pharmacology to map how glucocorticoid signaling shapes heart cell fate and regeneration potential. These findings lay the groundwork for future clinical strategies that might enhance recovery after myocardial infarction and reduce long-term heart failure risk. Attribution: Nature Cardiovascular Research for the primary report and related data.