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.
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.