Hua Linda Cai

Hua Cai

Professor, Anesthesiology, University of California Los Angeles

Professor, Medicine, University of California Los Angeles

(310) 267-2303

Mailing Address:
UCLA Department of Anesthesiology
757 Westwood Plaza, Suite 3325
Los Angeles, CA 90095

Work Address:
650 Charles E Young Dr, South
Los Angeles, CA 90095

Fax Number:
(310) 825-0132


Cai Laboratory

Department Website


Member, Molecular Medicine, Cell & Developmental Biology GPB Home Area, JCCC Signal Transduction and Therapeutics Program Area, Molecular Pharmacology GPB Home Area, Molecular, Cellular & Integrative Physiology GPB Home Area
Faculty, Medicine, Cardiovascular Research Lab

Research Interests

The Cai laboratory has long-term interests in molecular regulation of the cardiovascular protective enyzme endothelial nitric oxide synthase (eNOS), and contributions to cardiovascular diseases of increased reactive oxygen species production (ROS). ROS are a family of oxygen-derived molecules that are highly reactive to directly cause protein or DNA damage, or activate signal transduction pathways that are essential in disease initiation or progression. For example, one electron reduction of molecular oxygen results in formation of superoxide anion, which can ultra rapidly react with nitric oxide to result in formation of a more toxic oxidant peroxynitrite, and a loss in nitric oxide bioavailability and nitric oxide-dependent vasodilatation, as well as nitric oxide-dependent anti-inflammatory and anti-atherosclerotic functions. The goal of our research is to delineate details of eNOS regulation under oxidant stress environment, which may lead to novel therapeutics targeting an array of cardiovascular disorders including hypertension, atherosclerosis, diabetic vascular diseases, heart failure and biological process of aging. In deed, in the past few years our lab has discovered and characterized novel mechanisms whereby eNOS is dysfunctionally regulated to generate ROS itself, deteriorating oxidant stress [Proc Natl Acad Sci U S A. Track II (2005) 102(25):9056-61; Diabetes (2007) Jan 56(1):118-126; Am. J. Physiol. Heart Circ. Physiol. (2009) Jul;297(1):H331-9; J. Mol Cell Cardiol. (2009)]. Based on these findings are currently testing novel therapeutics in mouse models of hypertension and diabetes. These regiments are anticipated to restore eNOS function to hinder disease progression. Another major direction of research in our laboratory is to identify innovative pathways of vascular repair. Endothelium is the thin lay of endothelial cells lining the luminal surface of blood vessels. It represents the first line of defense protecting the blood vessels against blood-borne insults such as hormones (i.e. elevated angiotensin II in hypertensive patients), disturbed flow and inflammatory cytokines (released by inflammatory cells). Additionally, endothelium can be physically damaged during catheterization or endovascular surgeries. Without intact endothelium, the rest of the blood vessels can be damaged to cause severe vascular disorders. Thus our goal has been to identify and characterize novel vascular repair mechanisms that can lead to enhanced endothelial cell proliferation and migration, as well as accelerated wound closure. Some of the findings have been published in prestigious journals [Proc Natl Acad Sci U S A. (2006) Track II, Apr 25;103(17):6530-5; Circulation Research (2009);104:50-59] Our group is also interested in novel pathways mediating nitric oxide-dependent cardioprotection. We have recently shown that netrin-1 potently protects the heart from ischemia/reperfusion induced myocardial infarction via activation of DCC/NO/ERK1/2/eNOS/DCC feed-forward mechanism [J. Mol Cell Cardiol. (2010)]. We have projects ongoing to also investigate oxidant stress mechanisms in human atrial fibrillation, the most common cardiac arrhythmia; a role of vascular oxidative stress in obesity; and novel therapeutics eliminating cardiovascular side effects of cancer drugs.