Dr. Liao is a Professor of Medicine and co-Director of Stanford Cardiac Amyloid Center. The major goal of her research program focuses on understanding the mechanisms that underlie the pathophysiology of heart failure and developing novel treatments to combat this process. Her laboratory has played an international leading role in the study of amyloid light chain (AL) cardiomyopathy, a rare and fatal form of cardiovascular disease. We have described the underlying pathophysiologic basis for amyloid cardiomyopathy and found that the circulating amyloidogenic light chain proteins that characterize this disease directly result in a specific cardiotoxic response. Consequently, our research work has redefined AL cardiomyopathy and has raised new treatment approaches. More recently, her research efforts have expanded to include transthyretin (ATTR) cardiac amyloidosis.
In line with her goal of revealing novel therapeutic strategies for patients with cardiovascular disease, our efforts have also focused on characterizing and harnessing endogenous cardiac regenerative mechanisms. Her laboratory initially demonstrated the therapeutic potential of exogenous primitive muscle cells delivered to the injured heart. This work was among the earliest milestones in the field and served as the basis for an international trial of cell-based therapy. Subsequently, Liao lab identified and characterized a population of cardiac progenitor cells and its relationship and dynamic activity following cardiac injury in the adult heart. Her laboratory aims to reveal the molecular mechanisms regulating the endogenous regenerative capacity of the heart and to harness such repair mechanisms for the treatment of cardiovascular disease. Dr. Liao has lectured extensively on both amyloid cardiomyopathy and stem cell biology, and have maintained a history of independent NIH funding in these areas for more than two decades.
Over the course of her academic career, she has taken the greatest pride in mentoring the next generation of scientists. Dr. Liao has had the privilege to supervise several dozen students, postdoctoral fellows, and junior faculty, many of whom have gone on to independent academic careers at the highest institutions. Her contribution to the advancement of scientific knowledge also includes lecturing at various university and academic institutions as well as at scores of conferences and symposia locally, nationally, and internationally.
Co-Director, Stanford Amyloid Center (2017 - Present)
Boards, Advisory Committees, Professional Organizations
Associate Director, Cardiac Muscle Research Laboratory, Boston University School of Medicine (1997 - 2003)
Co-Director, Cardiac Muscle Research Laboratory, Boston University School of Medicine (2003 - 2005)
Director, Integrated Cardiovascular Physiology Laboratory, Department of Medicine, Boston University School of Medicine (2004 - 2005)
Director, Cardiac Muscle Research Laboratory, Department of Medicine, Brigham and Women’s Hospital (2005 - Present)
Director, Brigham and Women’s Hospital Cardiovascular Physiology Core (2010 - Present)
Vice Chair, Basic Cardiovascular Sciences Council, American Heart Association (2014 - 2016)
Chair, Basic Cardiovascular Sciences Council, American Heart Association (2016 - 2018)
Director, Brigham and Women’s Hospital Physiological NMR Core (2017 - Present)
Postdoc, Brigham and Women's Hospital and Harvard Medical School, Myocardial energetics (1991)
Postdoc, Beth Israel Hospital and Harvard Medical School, Cardiac physiology (1990)
M.A. (hon), Harvard University, Biomedical Science (2015)
PhD, University of Alabama at Birmingham, Biophysics (1990)
Zebrafish model of amyloid light chain cardiotoxicity: regeneration vs degeneration.
American journal of physiology. Heart and circulatory physiology
Cardiac dysfunction is the most frequent cause of morbidity and mortality in immunoglobulin light chain (AL) amyloidosis. Previously published transgenic animal models of AL amyloidosis have not recapitulated the key phenotype of cardiac dysfunction seen in AL amyloidosis which has limited our understanding of the disease mechanisms in vivo, as well as the development of targeted AL therapeutics. We have developed a transgenic zebrafish model in which a AL patient-derived lambda light chain (LC) is conditionally expressed in the liver under the control of UAS-Gal4 enhancer system. Circulating LC levels of 125 g/ml in these transgenic zebrafish are comparable to median pathologic serum LC levels. Functional analysis links abnormal contractile function with evidence of cellular and molecular proteotoxicity in the heart, including increased cell death and autophagy. However, despite pathologic and functional phenotypes analogous to human AL, the lifespan of the transgenic fish is comparable to control fish without the expressed AL-LC transgene. Nuclear labeling experiments suggest increased cardiac proliferation in the transgenic fish, which can be counteracted by treatment with a small molecule proliferation inhibitor leading to increased zebrafish mortality due to cardiac apoptosis and functional deterioration. This transgenic zebrafish model provides a platform to further study underlying AL disease mechanisms in vivo.
View details for DOI 10.1152/ajpheart.00788.2018
View details for PubMedID 30875258
Convergences of Life Sciences and Engineering in Understanding and Treating Heart Failure.
2019; 124 (1): 161–69
On March 1 and 2, 2018, the National Institutes of Health 2018 Progenitor Cell Translational Consortium, Cardiovascular Bioengineering Symposium, was held at the University of Alabama at Birmingham. Convergence of life sciences and engineering to advance the understanding and treatment of heart failure was the theme of the meeting. Over 150 attendees were present, and >40 scientists presented their latest work on engineering human functional myocardium for disease modeling, drug development, and heart failure research. The scientists, engineers, and physicians in the field of cardiovascular sciences met and discussed the most recent advances in their work and proposed future strategies for overcoming the major roadblocks of cardiovascular bioengineering and therapy. Particular emphasis was given for manipulation and using of stem/progenitor cells, biomaterials, and methods to provide molecular, chemical, and mechanical cues to cells to influence their identity and fate in vitro and in vivo. Collectively, these works are profoundly impacting and progressing toward deciphering the mechanisms and developing novel treatments for left ventricular dysfunction of failing hearts. Here, we present some important perspectives that emerged from this meeting.
View details for PubMedID 30605412