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Director, Division of Molecular Cardiovascular Biology
Co-Director, Heart Institute
Professor, UC Department of Pediatrics
I enjoy all areas of science but eventually focused on biological medical research. I find science fascinating and was always drawn to biomedical research. At Cincinnati Children’s — where I lead the Division of Molecular Cardiovascular Biology — I look for new molecular mechanisms of disease that might lead to new treatments.
My research interests include heart disease, muscular dystrophy, tissue fibrosis, calcium handling, ER stress signaling, cardiac hypertrophic signaling pathways and COVID-19 disease mechanisms.
Our laboratory has made significant contributions to the area of stem cell therapy for the heart. We have shown that presumed adult stem cells do not regenerate the heart. Instead, direct injection of these cells into the injured heart has a protective effect by altering the innate immune response and the activity of healing macrophages.
I have been a full investigator with the Howard Hughes Medical Institute since 2008. For my work, I have been awarded the Basic Research Prize from the American Heart Association.
I take great pride in helping young scientists who wish to pursue careers in biomedical research. Dozens of my past trainees have gone on to principle investigator roles at academic institutions.
Heart, Fibrosis, Molecular Cardiovascular Biology
Jeffery D. Molkentin, PhD, Ming Tan, PhD ...5/26/2020
Jeffery D. Molkentin, PhD6/30/2019
Jeffery D. Molkentin, PhD6/27/2019
BS: Marquette University, Milwaukee, WI, 1989.
PhD: Medical College of Wisconsin, 1994.
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.
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.
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