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Director, Division of Molecular Cardiovascular Biology
Co-Director, Heart Institute
Professor, UC Department of Pediatrics
Jeffery D. Molkentin, PhD, is a professor in the Department of Pediatrics at the University of Cincinnati and Cincinnati Children's Hospital Medical Center. He received his BS from Marquette University in Milwaukee Wisconsin (USA) in 1989. He then received his PhD from the Medical College of Wisconsin in 1994, after which he performed postdoctoral training with Dr. Eric Olson in Texas (USA) from 1994-1997, followed by his first faculty appointment in 1997 at the Cincinnati Children’s Hospital Medical Center of the University of Cincinnati (USA). Dr. Molkentin has published over 400 original articles during this time, he has a Scopus H-index of 111. Dr. Molkentin was a Pew Scholar early in his career and is now a full investigator of the Howard Hughes Medical Institute in the USA since 2008. He has also won several awards such as the Louis N and Arnold M Katz award to young investigators and more recently the Basic Research Prize, both of the American Heart Association. Dr. Molkentin also won the Lucian Award from McGill University. He has also served on NIH study section and was an organizer of various national and international scientific meetings. Finally, Dr Molkentin has placed 35 of his past trainees into academics as laboratory principle investigators. Dr. Molkentin’s research program continues to focus on the identification of candidate genes and signaling pathways involved in cardiac hypertrophy, contractility, cell death, heart failure, fibrosis, regeneration and muscular dystrophy, as well as mitochondria-dependent necrosis.
Heart, Fibrosis, Molecular Cardiovascular Biology
Jeffery D. Molkentin, PhD6/30/2019
Jeffery D. Molkentin, PhD6/27/2019
BS: Marquette University, Milwaukee, WI, 1989.
PhD: Medical College of Wisconsin, 1994.
Overlapping and differential functions of ATF6 alpha versus ATF6 beta in the mouse heart.
Correll, RN; Grimes, KM; Prasad, V; Lynch, JM; Khalil, H; Molkentin, JD.
Thrombospondin-3 augments injury-induced cardiomyopathy by intracellular integrin inhibition and sarcolemmal instability.
Schips, TG; Vanhoutte, D; Vo, A; Correll, RN; Brody, MJ; Khalil, H; Karch, J; Tjondrokoesoemo, A; Sargent, MA; Maillet, M; et al.
Inhibition of mitochondrial permeability transition by deletion of the ANT family and CypD.
Karch, J; Bround, MJ; Khalil, H; Sargent, MA; Latchman, N; Terada, N; Peixoto, PM; Molkentin, JD.
Cell-specific ablation of Hsp47 defines the collagen-producing cells in the injured heart.
Khalil, H; Kanisicak, O; Vagnozzi, RJ; Johansen, AK; Maliken, BD; Prasad, V; Boyer, JG; Brody, MJ; Schips, T; Kilian, KK; et al.
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.
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.
Genetic Lineage Tracing of Sca-1(+) Cells Reveals Endothelial but Not Myogenic Contribution to the Murine Heart.
Vagnozzi, RJ; Sargent, MA; Lin, SJ; Palpant, NJ; Murry, CE; Molkentin, JD.
The mitochondrial calcium uniporter underlies metabolic fuel preference in skeletal muscle.
Kwong, JQ; Huo, J; Bround, MJ; Boyer, JG; Schwanekamp, JA; Ghazal, N; Maxwell, JT; Jang, YC; Khuchua, Z; Shi, K; et al.
Gata4-Dependent Differentiation of c-Kit(+)-Derived Endothelial Cells Underlies Artefactual Cardiomyocyte Regeneration in the Heart.
Maliken, BD; Kanisicak, O; Karch, J; Khalil, H; Fu, X; Boyer, JG; Prasad, V; Zheng, Y; Molkentin, JD.
Undeniable Evidence That the Adult Mammalian Heart Lacks an Endogenous Regenerative Stem Cell.
Maliken, BD; Molkentin, JD.
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