Jeffery D. Molkentin

Last updated
Jeffery Daniel Molkentin
Jeffery D. Molkentin.jpg
Born (1967-01-15) January 15, 1967 (age 56)
NationalityAmerican
Alma materMarquette University
Scientific career
FieldsMolecular biology

Jeffery Daniel Molkentin (born January 15, 1967, in Milwaukee, Wisconsin) is an American molecular biologist. [1] He is the director of Molecular Cardiovascular Biology for Cincinnati Children's hospital where he is also co-director of their Heart Institute. [2] Molkentin holds a professorship at the University of Cincinnati's Department of Pediatrics. [3] [4]

Contents

Biography

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 a Scopus h-index of 130 and a Google Scholar h-index of 156. [9] [10] Molkentin is ranked 170th most cited Biology and Biochemistry researcher out of 30,000 scientists in the Research.com database. [11] His work has been published in several prestigious research journals, including "Nature", [12] "PNAS", [13] "Circulation Research", [14] and "Cell". [15]

Molkentin was a full investigator for the Howard Hughes Medical Institute (HHMI) from 2008 to 2021. [16]

Awards and honors

Selected publications

Related Research Articles

<span class="mw-page-title-main">Cardiac muscle</span> Muscular tissue of heart in vertebrates

Cardiac muscle is one of three types of vertebrate muscle tissues, with the other two being skeletal muscle and smooth muscle. It is an involuntary, striated muscle that constitutes the main tissue of the wall of the heart. The cardiac muscle (myocardium) forms a thick middle layer between the outer layer of the heart wall and the inner layer, with blood supplied via the coronary circulation. It is composed of individual cardiac muscle cells joined by intercalated discs, and encased by collagen fibers and other substances that form the extracellular matrix.

Hypertrophic cardiomyopathy is a condition in which muscle tissues of the heart become thickened without an obvious cause. The parts of the heart most commonly affected are the interventricular septum and the ventricles. This results in the heart being less able to pump blood effectively and also may cause electrical conduction problems. Specifically, within the bundle branches that conduct impulses through the interventricular septum and into the Purkinje fibers, as these are responsible for the depolarization of contractile cells of both ventricles.

<span class="mw-page-title-main">MYH7</span> Protein-coding gene in the species Homo sapiens

MYH7 is a gene encoding a myosin heavy chain beta (MHC-β) isoform expressed primarily in the heart, but also in skeletal muscles. This isoform is distinct from the fast isoform of cardiac myosin heavy chain, MYH6, referred to as MHC-α. MHC-β is the major protein comprising the thick filament that forms the sarcomeres in cardiac muscle and plays a major role in cardiac muscle contraction.

Alan W. Heldman is an American interventional cardiologist. Heldman graduated from Harvard College, University of Alabama School of Medicine, and completed residency and fellowship training at Johns Hopkins University School of Medicine. He held positions on the faculty of Johns Hopkins from 1995 to 2007. In 2007, he became clinical chief of cardiology at the University of Miami's Leonard M. Miller School of Medicine.

<span class="mw-page-title-main">PRKCE</span> Protein-coding gene in the species Homo sapiens

Protein kinase C epsilon type (PKCε) is an enzyme that in humans is encoded by the PRKCE gene. PKCε is an isoform of the large PKC family of protein kinases that play many roles in different tissues. In cardiac muscle cells, PKCε regulates muscle contraction through its actions at sarcomeric proteins, and PKCε modulates cardiac cell metabolism through its actions at mitochondria. PKCε is clinically significant in that it is a central player in cardioprotection against ischemic injury and in the development of cardiac hypertrophy.

<span class="mw-page-title-main">TNNI3</span> Protein-coding gene in the species Homo sapiens

Troponin I, cardiac muscle is a protein that in humans is encoded by the TNNI3 gene. It is a tissue-specific subtype of troponin I, which in turn is a part of the troponin complex.

<span class="mw-page-title-main">TNNT2</span> Protein-coding gene in the species Homo sapiens

Cardiac muscle troponin T (cTnT) is a protein that in humans is encoded by the TNNT2 gene. Cardiac TnT is the tropomyosin-binding subunit of the troponin complex, which is located on the thin filament of striated muscles and regulates muscle contraction in response to alterations in intracellular calcium ion concentration.

<span class="mw-page-title-main">ACTC1</span> Protein-coding gene in the species Homo sapiens

ACTC1 encodes cardiac muscle alpha actin. This isoform differs from the alpha actin that is expressed in skeletal muscle, ACTA1. Alpha cardiac actin is the major protein of the thin filament in cardiac sarcomeres, which are responsible for muscle contraction and generation of force to support the pump function of the heart.

<span class="mw-page-title-main">Myosin binding protein C, cardiac</span> Protein-coding gene in the species Homo sapiens

The myosin-binding protein C, cardiac-type is a protein that in humans is encoded by the MYBPC3 gene. This isoform is expressed exclusively in heart muscle during human and mouse development, and is distinct from those expressed in slow skeletal muscle (MYBPC1) and fast skeletal muscle (MYBPC2).

<span class="mw-page-title-main">Homeobox protein Nkx-2.5</span> Protein-coding gene in humans

Homeobox protein Nkx-2.5 is a protein that in humans is encoded by the NKX2-5 gene.

<i>TBX5</i> (gene) Protein-coding gene that affects limb development and heart and bone function

T-box transcription factor TBX5, is a protein that in humans is encoded by the TBX5 gene. Abnormalities in the TBX5 gene can result in altered limb development, Holt-Oram syndrome, Tetra-amelia syndrome, and cardiac and skeletal problems.

<span class="mw-page-title-main">MYH6</span> Protein-coding gene in the species Homo sapiens

Myosin heavy chain, α isoform (MHC-α) is a protein that in humans is encoded by the MYH6 gene. This isoform is distinct from the ventricular/slow myosin heavy chain isoform, MYH7, referred to as MHC-β. MHC-α isoform is expressed predominantly in human cardiac atria, exhibiting only minor expression in human cardiac ventricles. It is the major protein comprising the cardiac muscle thick filament, and functions in cardiac muscle contraction. Mutations in MYH6 have been associated with late-onset hypertrophic cardiomyopathy, atrial septal defects and sick sinus syndrome.

<span class="mw-page-title-main">Obscurin</span> Protein-coding gene in the species Homo sapiens

Obscurin is a protein that in humans is encoded by the OBSCN gene. Obscurin belongs to the family of giant sarcomeric signaling proteins that includes titin and nebulin. Obscurin is expressed in cardiac and skeletal muscle, and plays a role in the organization of myofibrils during sarcomere assembly. A mutation in the OBSCN gene has been associated with hypertrophic cardiomyopathy and altered obscurin protein properties have been associated with other muscle diseases.

<span class="mw-page-title-main">HAND2</span> Protein-coding gene in the species Homo sapiens

Heart- and neural crest derivatives-expressed protein 2 is a protein that in humans is encoded by the HAND2 gene.

<span class="mw-page-title-main">CSRP3</span> Protein-coding gene in the species Homo sapiens

Cysteine and glycine-rich protein 3 also known as cardiac LIM protein (CLP) or muscle LIM protein (MLP) is a protein that in humans is encoded by the CSRP3 gene.

<span class="mw-page-title-main">MYL7</span> Protein-coding gene in the species Homo sapiens

Atrial Light Chain-2 (ALC-2) also known as Myosin regulatory light chain 2, atrial isoform (MLC2a) is a protein that in humans is encoded by the MYL7 gene. ALC-2 expression is restricted to cardiac muscle atria in healthy individuals, where it functions to modulate cardiac development and contractility. In human diseases, including hypertrophic cardiomyopathy, dilated cardiomyopathy, ischemic cardiomyopathy and others, ALC-2 expression is altered.

<span class="mw-page-title-main">Hugh Christian Watkins</span>

Hugh Christian Watkins is a British cardiologist. He is a Fellow of Merton College, Oxford, an associate editor of Circulation Research, and was Field Marshal Alexander Professor of Cardiovascular Medicine in the University of Oxford between 1996 and 2013.

A bioartificial heart is an engineered heart that contains the extracellular structure of a decellularized heart and cellular components from a different source. Such hearts are of particular interest for therapy as well as research into heart disease. The first bioartificial hearts were created in 2008 using cadaveric rat hearts. In 2014, human-sized bioartificial pig hearts were constructed. Bioartificial hearts have not been developed yet for clinical use, although the recellularization of porcine hearts with human cells opens the door to xenotransplantation.

<span class="mw-page-title-main">Ischemic cardiomyopathy</span> Medical condition

Ischemic cardiomyopathy is a type of cardiomyopathy caused by a narrowing of the coronary arteries which supply blood to the heart. Typically, patients with ischemic cardiomyopathy have a history of acute myocardial infarction, however, it may occur in patients with coronary artery disease, but without a past history of acute myocardial infarction. This cardiomyopathy is one of the leading causes of sudden cardiac death. The adjective ischemic means characteristic of, or accompanied by, ischemia — local anemia due to mechanical obstruction of the blood supply.

Roberta Anne Gottlieb is an American oncologist, academic, and researcher. She is a Professor, and Vice-Chair of Translational Medicine in the Department of Biomedical Sciences at Cedars-Sinai Medical Center, and a Professor of Medicine at the University of California, Los Angeles.

References

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  5. "Regulation of Cardiac Hypertrophy | Molkentin Lab". www.cincinnatichildrens.org. Retrieved 2021-01-03.
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  8. Johnson, Carolyn Y. "Benefits of stem cell heart therapy may have nothing to do with stem cells, a study on mice suggests". Washington Post. ISSN   0190-8286 . Retrieved 2021-01-03.
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  13. Karch, J.; Molkentin, J. D. (2014-07-07). "Identifying the components of the elusive mitochondrial permeability transition pore". Proceedings of the National Academy of Sciences. 111 (29): 10396–10397. Bibcode:2014PNAS..11110396K. doi: 10.1073/pnas.1410104111 . ISSN   0027-8424. PMC   4115577 . PMID   25002521.
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