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Heart Repair in Mice Researchers compared genes active in the hearts of newborn mice after a heart attack and after aortic constriction. A combination of three proteins, mainly secreted by immune cells in the heart, reduced cell death and increased cell division in cellular experiments. Both effects required TLR2, a sensor protein on the surface of heart cells. In adult hearts, heart cells are rarely renewed. In mice, there is a short window after birth when these contracting muscle cells still divide. A previous study by the same group in 2019 found that aortic constriction on the first day of life preserved heart function and was accompanied by capillary growth. If performed on the seventh day, heart function deteriorated and fibrosis occurred. The new study sought signals that trigger early heart repair under such stress. The authors compared genes active one day after a heart attack induced on the first day of life with genes active after two weeks of aortic constriction. Among 995 common genes, they selected three proteins secreted into the surrounding tissue: CCL4, S100A8, and C1QA. These proteins have receptors on heart cells and vessel cells, and tissue staining showed that they are mainly produced by immune cells in the heart after stress. 🔗 Read original →