CTSA News

A protein famous for stunting tumor growth might seem out of place in a discussion about heart disease and scarring, but research supported in part by the University of Rochester (UR) CTSI suggests that the tumor suppressor protein p53 might play an important role in both. University of Rochester Medical Center researchers believe that having too much p53 may speed progression of a disease marked by loss of heart muscle, while having too little p53 could tip the scales from repair to harmful scarring after a cardiac injury such as a heart attack.

Absence (of p53) Makes the Heart Grow Firmer

Scarring of the heart, also called cardiac fibrosis, happens when the mechanisms meant to repair heart tissue run amok. In response to injury, cells called fibroblasts begin multiplying and secreting a scaffold of molecules that help patch and repair damaged tissue. If too many fibroblasts are created and too much of that scaffolding, called extracellular matrix, is released, the heart begins to scar and become rigid, impeding its ability to pump normally…

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