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Significance Heart disease is associated with the development of fibrosis, a type of scarring that impedes cardiac function. The primary cellular source of cardiac fibrosis is the resident cardiac fibroblast. We found that cardiac fibroblasts from human heart failure patients or a mouse model of heart disease express excessive amounts of the SPRR2B protein. We provide evidence that SPRR2B is a signal-responsive regulatory subunit of the p53 ubiquitination complex that stimulates the destruction of p53 and the accumulation of pathological fibroblasts. This study defines a unique mechanism of cell cycle control that is dysfunctional in heart disease and may drive the development pathological fibrosis.

Small proline-rich protein 2B drives stress-dependent p53 degradation and fibroblast proliferation in heart failure