Dr. Daniel Bernstein completed his undergraduate education at MIT and his MD at NYU. He did his pediatric residency at Montefiore Medical Center in New York, a Fellowship in Medical Education at the Albert Einstein College of Medicine and then a fellowship in Pediatric Cardiology at the UCSF, under the mentorship of Dr. Abraham Rudolph. He joined the faculty at Stanford in 1986, served as Chief of Pediatric Cardiology from 1994-2011 and as Director of the Children’s Heart Center at Packard Children’s Hospital from 2001-2011. In 2018 he was appointed Associate Dean for Curriculum and Scholarship at the Stanford School of Medicine, where he oversees medical student education and research.
Dr. Bernstein has directed an NIH- and AHA-funded basic science lab for over 35 years, focusing on how cell signaling regulates the balance between cardiotoxicity and cardioprotection. Together with Brian Kobilka, he was part of a team that created some of the first murine gene knockouts and he spent the next decade studying the role of β-adrenergic receptors in regulating cardiac function in health and disease. His more recent work applies the powerful tools of CRISPR gene editing and patient-derived induced pluripotent stem cells (iPSCs) to study the mechanisms of heart disease, including hypertrophic cardiomyopathy, and to enhance the power of pharmacogenomics to screen patients for susceptibility to drug toxicity. Dr. Bernstein has also been at the forefront of pediatric heart failure and transplantation since the infancy of both fields. He published the first proof that the transplanted heart grows as the child grows, one of the first descriptions of post-transplant tumors, and transplantation for children born with congenital heart disease. He has led several multi-center clinical trials in pediatric solid organ transplantation.
Dr. Bernstein's research program focuses on regulation of cardiovascular function in both normal physiologic states as well as in disease states such as cardiomyopathy. Their major focus at this time is on hypertrophic cardiomyopathy (HCM) and how mutations in sarcomeric proteins such as α-myosin lead to alterations in cellular physiology and morphology. Over the past two decades they have gained substantial insight into the genes that are responsible for HCM, however, despite this knowledge, there are still many unanswered questions on how these mutations translate into the clinical phenotypes seen in patients.
