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Haiming Cao, Ph.D.

Laboratory of Obesity and Metabolic Diseases

Haiming Cao
Haiming Cao, Ph.D.
Earl Stadtman Investigator
Laboratory of Obesity and Metabolic Diseases
Building 10 Room 8N109
Bethesda, MD 20892
P: +1 (301) 402-9032
F: +1 (301) 480-0360
caoh3@nhlbi.nih.gov

Background

Haiming Cao earned his Ph.D. in biochemistry in 2003 from the University of Nevada Reno. He did his postdoctoral training at Harvard University from 2003 to 2010. Dr. Cao joined the NHLBI as an Earl Stadtman 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.

Most recently, the Cao group has identified a large number of long noncoding RNAs that could function as vital signaling and metabolic regulators in mammals (Cell Metab. 2015 March 3, 21(3): 455–467) and might constitute a new class of RNA therapeutic targets for diseases. Dr. Cao’s team is currently 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

A Liver-Enriched Long Non-Coding RNA, lncLSTR, Regulates Systemic Lipid Metabolism in Mice.
Li P, Ruan X, Yang L, Kiesewetter K, Zhao Y, Luo H, Chen Y, Gucek M, Zhu J, Cao H
Cell Metab 2015 Mar 3;21(3):455-67.
Adipocyte lipid chaperone AP2 is a secreted adipokine regulating hepatic glucose production.
Cao H, Sekiya M, Ertunc ME, Burak MF, Mayers JR, White A, Inouye K, Rickey LM, Ercal BC, Furuhashi M, Tuncman G, Hotamisligil GS
Cell Metab 2013 May 7;17(5):768-78.
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.
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.
Haiming Cao's Full List of Publications