Abstract

Born in Salzwedel, East Germany, Matthias Nahrendorf entered adulthood just as the Iron Curtain was lifting in Eastern Europe. He earned his medical degree and PhD in cardiovascular biology at Heidelberg University, and completed his residency plus fellowships in internal medicine and cardiovascular imaging at University of Wuerzburg. In 2004, a postdoctoral position at Massachusetts General Hospital’s Center for Molecular Imaging Research brought Nahrendorf to Boston. He is now a principal investigator at MGH’s Center for Systems Biology and director of the hospital’s Mouse Imaging Program. Nahrendorf, 45, is pursuing a deeper understanding of the consequences of ischemic injury, especially regarding how monocytes/macrophages impact acute healing and scar development,1–3 and how an imbalance in the process fuels prolonged inflammation and then heart failure. An associate professor of radiology at Harvard Medical School, Nahrendorf and his collaborators are also developing molecular imaging tools to noninvasively study regulators of heart failure biology and infarct healing processes.4–6 A long-term goal of the work is to devise new therapies for ischemic injury that reduce the action of inflammatory cells to what is necessary only to promote healthy healing, Nahrendorf says. If that could be achieved, “Ideally we wouldn’t have heart failure anymore.” I have one brother, he’s younger, and my parents. It was a pretty sheltered childhood. I grew up in Magdeburg, and the (Berlin) Wall came down when I was 18. Army service was compulsory in East Germany. So I spent one year in the army and then Germany reunited, so I was free to go wherever I wanted. My parents are both doctors. My dad is a cardiologist, my mom a pediatrician. I had a happy childhood. They were never telling me what to do. But I was obviously influenced by their jobs. They talked about …

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