Kathryn Moore

Last updated
Kathryn J. Moore
Kathryn Moore2.jpg
Alma mater McGill University
Known forAtherosclerosis
AwardsNational Institutes of Health R35 Outstanding Investigator Award

Fellow of the National Academy of Sciences

American Heart Association Distinguished Scientist Award
Scientific career
FieldsAtherosclerosis and Inflammation
Institutions Harvard Medical School
New York University Langone Medical Center
Thesis Regulation of macrophage function during intracellular infection with Leishmania donovani.  (1994)
Doctoral advisor Greg Matlashewski
Website https://kathrynmoorelab.com/

Kathryn J. Moore is a Canadian-born American biomedical scientist and cell biologist. She is the Jean and David Blechman Professor of Cardiology and the founding director of the Cardiovascular Research Center [1] at the New York University Grossman School of Medicine. Moore's research considers the pathogenesis of atherosclerosis, with a focus on the identification of novel therapeutic targets. She was elected Fellow of the National Academy of Sciences in 2021. [2]

Contents

Early life and education

Kathryn Moore was born in Montreal, Quebec, Canada, where she attended McGill University. Moore studied microbiology, receiving her BSc (Distinction) from McGill University in 1989. She remained there for graduate studies, studying mechanisms by which the intracellular pathogen Leishmania donovani subverts macrophage microbicidal functions, [3] [4] [5] under the Canadian immunologist Greg Matlashewski. Moore was awarded her PhD in parasitology in 1994. [6]

Research and career

Moore joined the Harvard Medical School faculty as an Instructor in Medicine in 1999 and was promoted to Assistant Professor in 2002. Her early research focused on innate immune mechanisms of chronic inflammation in age-related diseases such as atherosclerosis and Alzheimer’s Disease. [7] [8]

In 2009, Moore was recruited to the New York University Langone Medical Center, where she continued to focus on origins of cardiovascular and metabolic diseases, in particular the roles that chronic inflammation and lipid dysregulation play in these processes. [9] She contributed to seminal studies showing that cholesterol crystals in atherosclerotic plaques cause lysosomal damage that activates the NLRP3 inflammasome to promote the maturation and release of interleukin-1b. [8]

Awards and honors

Related Research Articles

<i>Leishmania</i> Genus of parasitic flagellate protist

Leishmania is a parasitic protozoan, a single-celled organism of the genus Leishmania that is responsible for the disease leishmaniasis. They are spread by sandflies of the genus Phlebotomus in the Old World, and of the genus Lutzomyia in the New World. At least 93 sandfly species are proven or probable vectors worldwide. Their primary hosts are vertebrates; Leishmania commonly infects hyraxes, canids, rodents, and humans.

<span class="mw-page-title-main">Atherosclerosis</span> Inflammatory disease involving buildup of lesions in the walls of arteries

Atherosclerosis is a pattern of the disease arteriosclerosis, characterized by development of abnormalities called lesions in walls of arteries. This is a chronic inflammatory disease involving many different cell types, and driven by elevated levels of cholesterol in the blood. These lesions may lead to narrowing of the arterial walls due to buildup of atheromatous plaques. At onset there are usually no symptoms, but if they develop, symptoms generally begin around middle age. In severe cases, it can result in coronary artery disease, stroke, peripheral artery disease, or kidney disorders, depending on which body part(s) the affected arteries are located in the body.

<span class="mw-page-title-main">C-reactive protein</span> Mammalian protein found in humans

C-reactive protein (CRP) is an annular (ring-shaped) pentameric protein found in blood plasma, whose circulating concentrations rise in response to inflammation. It is an acute-phase protein of hepatic origin that increases following interleukin-6 secretion by macrophages and T cells. Its physiological role is to bind to lysophosphatidylcholine expressed on the surface of dead or dying cells in order to activate the complement system via C1q.

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NADPH oxidase is a membrane-bound enzyme complex that faces the extracellular space. It can be found in the plasma membrane as well as in the membranes of phagosomes used by neutrophil white blood cells to engulf microorganisms. Human isoforms of the catalytic component of the complex include NOX1, NOX2, NOX3, NOX4, NOX5, DUOX1, and DUOX2.

<span class="mw-page-title-main">Visceral leishmaniasis</span> Human disease caused by protist parasites

Visceral leishmaniasis (VL), also known as kala-azar or "black fever", is the most severe form of leishmaniasis and, without proper diagnosis and treatment, is associated with high fatality. Leishmaniasis is a disease caused by protozoan parasites of the genus Leishmania.

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<span class="mw-page-title-main">Paul Ridker</span> American epidemiologist and academic

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<i>Leishmania donovani</i> Species of intracellular parasite

Leishmania donovani is a species of intracellular parasites belonging to the genus Leishmania, a group of haemoflagellate kinetoplastids that cause the disease leishmaniasis. It is a human blood parasite responsible for visceral leishmaniasis or kala-azar, the most severe form of leishmaniasis. It infects the mononuclear phagocyte system including spleen, liver and bone marrow. Infection is transmitted by species of sandfly belonging to the genus Phlebotomus in Old World and Lutzomyia in New World. The species complex it represents is prevalent throughout tropical and temperate regions including Africa, China, India, Nepal, southern Europe, Russia and South America. The species complex is responsible for thousands of deaths every year and has spread to 88 countries, with 350 million people at constant risk of infection and 0.5 million new cases in a year.

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<span class="mw-page-title-main">Peter Tontonoz</span>

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References

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  2. 1 2 "2021 NAS Election". www.nasonline.org. Retrieved 2021-05-03.
  3. Moore, K. J.; Labrecque, S.; Matlashewski, G. (1993-05-15). "Alteration of Leishmania donovani infection levels by selective impairment of macrophage signal transduction". Journal of Immunology. 150 (10): 4457–4465. ISSN   0022-1767. PMID   8482844.
  4. Moore, K. J.; Turco, S. J.; Matlashewski, G. (Jan 1994). "Leishmania donovani infection enhances macrophage viability in the absence of exogenous growth factor". Journal of Leukocyte Biology. 55 (1): 91–98. doi:10.1002/jlb.55.1.91. ISSN   0741-5400. PMID   8283144.
  5. Moore, K. J.; Matlashewski, G. (1994-03-15). "Intracellular infection by Leishmania donovani inhibits macrophage apoptosis". Journal of Immunology. 152 (6): 2930–2937. ISSN   0022-1767. PMID   8144893.
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