Nancy Andrews

Positions:

Nanaline H. Duke Professor of Pediatrics

Pediatrics
School of Medicine

Dean Emerita of the School of Medicine

School of Medicine
School of Medicine

Professor of Pediatrics

Pediatrics
School of Medicine

Professor of Pharmacology & Cancer Biology

Pharmacology & Cancer Biology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

B.S. 1980

Yale University

M.S. 1980

Yale University

Ph.D. 1985

Massachusetts Institute of Technology

M.D. 1987

Harvard University

Grants:

School of Medicine 2017 Biddle

Administered By
School of Medicine
Awarded By
Mary Duke Biddle Foundation
Role
Principal Investigator
Start Date
End Date

NRSA Predoctoral Fellowship

Administered By
Sarah Stedman Nutrition & Metabolism Center
Awarded By
National Institutes of Health
Role
Principal Investigator
Start Date
End Date

Expansion of Animal Resources for Large Animals (Vivarium Expansion project)

Administered By
School of Medicine
Awarded By
National Institutes of Health
Role
Principal Investigator
Start Date
End Date

Genes that modify Iron loading in mice

Administered By
Pharmacology & Cancer Biology
Awarded By
National Institutes of Health
Role
Principal Investigator
Start Date
End Date

Identification of Novel Genes That Modulate Systemic Iron Homeostasis

Administered By
Pathology
Awarded By
National Institutes of Health
Role
Mentor
Start Date
End Date

Publications:

Lethal Cardiomyopathy in Mice Lacking Transferrin Receptor in the Heart.

Both iron overload and iron deficiency have been associated with cardiomyopathy and heart failure, but cardiac iron utilization is incompletely understood. We hypothesized that the transferrin receptor (Tfr1) might play a role in cardiac iron uptake and used gene targeting to examine the role of Tfr1 in vivo. Surprisingly, we found that decreased iron, due to inactivation of Tfr1, was associated with severe cardiac consequences. Mice lacking Tfr1 in the heart died in the second week of life and had cardiomegaly, poor cardiac function, failure of mitochondrial respiration, and ineffective mitophagy. The phenotype could only be rescued by aggressive iron therapy, but it was ameliorated by administration of nicotinamide riboside, an NAD precursor. Our findings underscore the importance of both Tfr1 and iron in the heart, and may inform therapy for patients with heart failure.
Authors
Xu, W; Barrientos, T; Mao, L; Rockman, HA; Sauve, AA; Andrews, NC
MLA Citation
Xu, Wenjing, et al. “Lethal Cardiomyopathy in Mice Lacking Transferrin Receptor in the Heart..” Cell Rep, vol. 13, no. 3, Oct. 2015, pp. 533–45. Pubmed, doi:10.1016/j.celrep.2015.09.023.
URI
https://scholars.duke.edu/individual/pub1091577
PMID
26456827
Source
pubmed
Published In
Cell Reports
Volume
13
Published Date
Start Page
533
End Page
545
DOI
10.1016/j.celrep.2015.09.023

Personalized medicine to anticipatory health

Authors
Andrews, NC
MLA Citation
Andrews, N. C. “Personalized medicine to anticipatory health.” Journal of Surgical Radiology, vol. 2, no. 3, Dec. 2011, pp. 220–23.
URI
https://scholars.duke.edu/individual/pub757608
Source
scopus
Published In
Journal of Surgical Radiology
Volume
2
Published Date
Start Page
220
End Page
223

Can we keep the "academic" in academic medicine? 2009 American Society for Clinical Investigation Presidential Address.

Authors
Andrews, NC
MLA Citation
Andrews, Nancy C. “Can we keep the "academic" in academic medicine? 2009 American Society for Clinical Investigation Presidential Address..” J Clin Invest, vol. 120, no. 1, Jan. 2010, pp. 390–93. Pubmed, doi:10.1172/JCI41934.
URI
https://scholars.duke.edu/individual/pub757615
PMID
20038792
Source
pubmed
Published In
J Clin Invest
Volume
120
Published Date
Start Page
390
End Page
393
DOI
10.1172/JCI41934

Climbing through medicine's glass ceiling.

Authors
Andrews, NC
MLA Citation
Andrews, Nancy C. “Climbing through medicine's glass ceiling..” N Engl J Med, vol. 357, no. 19, Nov. 2007, pp. 1887–89. Pubmed, doi:10.1056/NEJMp078198.
URI
https://scholars.duke.edu/individual/pub757630
PMID
17989380
Source
pubmed
Published In
The New England Journal of Medicine
Volume
357
Published Date
Start Page
1887
End Page
1889
DOI
10.1056/NEJMp078198

Chronic hepcidin induction causes hyposideremia and alters the pattern of cellular iron accumulation in hemochromatotic mice.

We report the generation of a tetracycline-regulated (Tet ON) transgenic mouse model for acute and chronic expression of the iron regulatory peptide hepcidin in the liver. We demonstrate that short-term and long-term tetracycline-dependent activation of hepcidin in adult mice leads to hypoferremia and iron-limited erythropoiesis, respectively. This clearly establishes the key role of hepcidin in regulating the extracellular iron concentration. We previously demonstrated that, when expressed early in fetal development, constitutive transgenic hepcidin expression prevented iron accumulation in an Hfe-/- mouse model of hemochromatosis. We now explore the effect of chronic hepcidin expression in adult Hfe-/- mice that have already developed liver iron overload. We demonstrate that induction of chronic hepcidin expression in 2-month-old Hfe-/- mice alters their pattern of cellular iron accumulation, leading to increased iron in tissue macrophages and duodenal cells but less iron in hepatocytes. These hepcidin-induced changes in the pattern of cellular iron accumulation are associated with decreased expression of the iron exporter ferroportin in macrophages but no detectable alteration of ferroportin expression in the hepatocytes. We speculate that this change in iron homeostasis could offer a therapeutic advantage by protecting against damage to parenchymal cells.
Authors
Viatte, L; Nicolas, G; Lou, D-Q; Bennoun, M; Lesbordes-Brion, J-C; Canonne-Hergaux, F; Schönig, K; Bujard, H; Kahn, A; Andrews, NC; Vaulont, S
MLA Citation
Viatte, Lydie, et al. “Chronic hepcidin induction causes hyposideremia and alters the pattern of cellular iron accumulation in hemochromatotic mice..” Blood, vol. 107, no. 7, Apr. 2006, pp. 2952–58. Pubmed, doi:10.1182/blood-2005-10-4071.
URI
https://scholars.duke.edu/individual/pub757644
PMID
16339398
Source
pubmed
Published In
Blood
Volume
107
Published Date
Start Page
2952
End Page
2958
DOI
10.1182/blood-2005-10-4071