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Haiming Cao, Ph.D.

Laboratory of Obesity and Metabolic Diseases

Haiming Cao, Ph.D.
Earl Stadtman Investigator
Laboratory of Obesity and Metabolic Diseases

Building 10 Room 8N109
10 Center Dr
Bethesda, MD 20892
P: +1 301 402 9032
F: +1 301 480 0360


Haiming Cao graduated with an M.S. in genetics from Harbin Normal University in China in 1997 and earned his Ph.D. in biochemistry in 2003 from the University of Nevada School of Medicine in Reno. He did his postdoctoral training at the School of Public Health at Harvard University from 2003 to 2010. Dr. Cao joined the NHLBI as a tenure-track Investigator in 2011.

Research Interests

The broad interest of the Cao group is to understand the molecular and pathophysiological basis of complex human diseases including but not limited to obesity, diabetes, fatty liver disease, and cardiovascular disease. The long-term goal of the lab is to bridge the gaps between new developments in molecular biology and diseases of significant public health impact and identify novel therapeutic interventions against complex human diseases.

The worldwide obesity epidemic, along with an array of obesity-related disorders, particularly diabetes, fatty liver and cardiovascular diseases, has become a major public health threat in the 21st century. Yet the molecular and pathological mechanisms by which obesity induces metabolic disorders remain incompletely understood, hampering the development of effective therapies against these debilitating diseases. The Cao group investigates the molecular and pathological basis of defective metabolism as a general cause of complex human diseases, using high-throughput sequencing, proteomic screens, and robust cell assays in combination with advanced bioinformatics analyses to identify critical metabolic regulators.

More recently, Dr. Cao has become particularly interested in the roles of long non-coding RNAs (lncRNAs) and epigenetic modifiers in metabolic disorders. Dr. Cao’s team is studying the pathophysiological significance of lncRNAs and epigenetic modifications in genetic and diseased animal models using a variety of high-throughput technologies; their direct implications in human diseases are further corroborated by studying patient samples from the NIH clinical center.

The efforts of numerous genome wide association studies (GWAS) in recent years have established a catalog of gene mutations that underlie human genetic diseases, including many metabolic disorders; this genetic information provides an unprecedented opportunity to develop therapies against these disorders on a knowledge basis. Dr. Cao’s group has obtained skin fibroblasts from patients carrying mutations that cause several metabolic disorders and have converted these cells into induced pluripotent stem (iPS) cells. They have differentiated these patient-specific iPS cells into metabolic cells such as cardiomyocytes and adipocytes and are screening for altered metabolic pathways and adipocytokine production in these functional metabolic cells. They will also confirm the pathological role of these mutations in immunodeficient mice that are engrafted with control and mutant cells. Establishing the physiological consequences of these metabolic mutations will pave the way for potential treatment strategies.

Selected Publications

Double-stranded RNA-dependent protein kinase links pathogen sensing with stress and metabolic homeostasis.
Nakamura T, Furuhashi M, Li P, Cao H, Tuncman G, Sonenberg N, Gorgun CZ, Hotamisligil GS.
Cell. 2010 Feb 5;140(3):338-48.
[Text Abstract on PubMed]

Identification of a lipokine, a lipid hormone linking adipose tissue to systemic metabolism.
Cao H, Gerhold K, Mayers JR, Wiest MM, Watkins SM, Hotamisligil GS.
Cell. 2008 Sep 19;134(6):933-44.
[Text Abstract on PubMed]

Regulation of metabolic responses by adipocyte/macrophage Fatty Acid-binding proteins in leptin-deficient mice.
Cao H, Maeda K, Gorgun CZ, Kim HJ, Park SY, Shulman GI, Kim JK, Hotamisligil GS.
Diabetes. 2006 Jul;55(7):1915-22.
[Text Abstract on PubMed]

Adipocyte/macrophage fatty acid binding proteins control integrated metabolic responses in obesity and diabetes.
Maeda K, Cao H, Kono K, Gorgun CZ, Furuhashi M, Uysal KT, Cao Q, Atsumi G, Malone H, Krishnan B, Minokoshi Y, Kahn BB, Parker RA, Hotamisligil GS.
Cell Metab. 2005 Feb;1(2):107-19.
[Text Abstract on PubMed]

A phosphotyrosine-dependent protein interaction screen reveals a role for phosphorylation of caveolin-1 on tyrosine 14: recruitment of C-terminal Src kinase.
Cao H, Courchesne WE, Mastick CC.
J. Biol. Chem. 2002 Mar 15;277(11):8771-4.
[Text Abstract on PubMed]

Haiming Cao's Full List of Publications

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Last Updated: April 26, 2013