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Heart attack: Inhibiting cell contact protein may limit damage During a heart attack the death of heart muscle cells causes lesions that transform into fibrotic tissue. Restricting the damage is critical, as mamalian heart muslce does not regenerate. The cell contact protein CAR, is upregulated in tissue surrounding lesions, but it has remained unclear if this part of the pathology or an attempt to contain the lesion. Michael Gotthardt at the Max-Delbrück-Center for Molecular Medicine in Berlin, Germany, and co-workers, examined CAR’s role following heart attack in CAR-inactivated and control mice. CAR exacerbates responses to low oxygen conditions and boosts a protein involved in cell death. The hearts of CAR-inactivated mice were not as enlarged as those of controls, and lesions were smaller and less fibrotic. Importantly, CAR deficiency improved survival, suggesting CAR inhibition as a suitable therapeutic strategy for patients with myocardial infarction.