Jeffery D. Molkentin

Molkentin was born and raised in Milwaukee, Wisconsin.,[1] where he attended Marquette University, receiving a B.S. in biology in 1989. He began studies to be a medical doctor at the University of Wisconsin,[2] but switched to a research program, and received his PhD in physiology from the Medical College of Wisconsin in 1994.[1]

Molkentin's work focuses on heart disease and muscular dystrophy, though he is involved in other types of research entailing calcium handling, ER stress signaling, cardiac hypertrophic signaling pathways,[5] and COVID-19 disease mechanisms.[6] One of Molkentin's most notable research achievements was his contribution to stem cell therapy in the heart and his disproving prior research about the topic.[7][8]

Molkentin is among the most highly cited researchers in the world, with his publications being cited over 50,000 times in literature.[9] His work has been published in several prestigious research journals, including "Nature",[10] "PNAS",[11] and "Circulation Research".[12]

Molkentin has been a full investigator for the Howard Hughes Medical Institute (HHMI) from 2008 to 2021.[13]

• 1998 Pew Scholar in the Biomedical Sciences[14]
• 2012 AHA Basic Science Research Prize[15]
• 2015 Lucian Award[15]
• 2019 AHA Merit Award Winner[16][17]

• MCUb induction protects the heart from postischemic remodeling. Huo, J; Lu, S; Kwong, JQ; Bround, MJ; Grimes, KM; Sargent, MA; Brown, ME; Davis, ME; Bers, DM; Molkentin, JD. Circulation Research. 2020; 127:379-390.
• An acute immune response underlies the benefit of cardiac stem cell therapy. Vagnozzi, RJ; Maillet, M; Sargent, MA; Khalil, H; Johansen, AK Z; Schwanekamp, JA; York, AJ; Huang, V; Nahrendorf, M; Sadayappan, S; et al. Nature. 2020; 577:405-409.
• Disruption of valosin-containing protein activity causes cardiomyopathy and reveals pleiotropic functions in cardiac homeostasis. Brody, MJ; Vanhoutte, D; Bakshi, CV; Liu, R; Correll, RN; Sargent, MA; Molkentin, JD. The Journal of biological chemistry. 2019; 294:8918-8929.
• ERK1/2 signaling induces skeletal muscle slow fiber-type switching and reduces muscular dystrophy disease severity. Boyer, JG; Prasad, V; Song, T; Lee, D; Fu, X; Grimes, KM; Sargent, MA; Sadayappan, S; Molkentin, JD. JCI insight. 2019; 5.