Manfred Boehm, M.D.
Manfred Boehm, M.D., is an investigator in the Center for Molecular Medicine at the National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health (NIH). He joined the NHLBI as a research fellow in 1999 and has been an NHLBI investigator since 2003.
Dr. Boehm’s primary research interests are in vascular biology and the genetics of vascular remodeling in human diseases. His group developed complex animal models and patient-specific disease models, including induced pluripotent stem cell-based systems, to understand the cellular and molecular mechanisms of vascular remodeling in rare or unknown inherited and acquired vascular diseases. His team revealed new signaling pathways pivotal for balanced vascular wound repair, described a new concept of cellular contributions during vascular remodeling and identified a new inherited vascular disease that causes arterial calcifications in adults. A more comprehensive knowledge of the cellular contributions and pathways involved in vascular remodeling will be critical for understanding this complex process and for the development of potential therapeutic applications in regenerative medicine.
Dr. Boehm received his Doctor of Medicine in 1993 from the University of Heidelberg, Germany and did a residency in internal medicine at the Franz-Volhard-Clinic in Berlin. Before arriving at the NHLBI, he was a research fellow at the Max-Delbrueck-Center for Molecular Medicine, Berlin (1996-1997) and University of Michigan, Ann Arbor (1997-1999). Dr. Boehm has authored numerous original scientific articles, reviews and book chapters, and has received many honors, including an NHLBI Star Award for Excellence in Laboratory Basic and Clinical Research in 2010.
Areas of expertise: blood vessel biology and diseases.
Dr. Boehm In the News
National Institutes of Health researchers have identified a biological pathway that contributes to the high rate of vein graft failure following bypass surgery. Using mouse models of bypass surgery, they showed that excess signaling via the Transforming Growth Factor Beta (TGF-Beta) family causes the inner walls of the vein become too thick, slowing down or sometimes even blocking the blood flow that the graft was intended to restore. Inhibition of the TGF-B signaling pathway reduced overgrowth in the grafted veins.
The NHLBI's Dr. Manfred Boehm reflects on the success of the NIH's Undiagnosed Diseases Program. The major initiative is temporarily postponing new applications but continues to investigate the unsolved diseases already in the queue.