BBS Faculty Member - Ronglih Liao

Ronglih Liao

Department of Medicine

Brigham and Women's Hospital
New Research Building, Room 431
77 Avenue Louis Pasteur
Boston, MA 02115
Tel: 617-525-4854
Fax: 617-525-4868
Lab Members: 4 postdoctoral fellows, 3 graduate students, 2 junior faculty, 2 research assistants

Following tissue injury or genetic alteration, the heart undergoes a process of molecular and structural remodeling, ultimately resulting in cardiac dysfunction. The central focus of our laboratory’s research is to understand the molecular mechanisms that mediate the transition from a normal to failing heart. Our research approaches attempt to bridge the growing span between basic bench research and patient care, with a goal towards identifying novel therapeutic targets for rapid translation into clinical medicine. We tackle these scientific interests by utilizing an integrated approach combining molecular studies with intensive investigation of cardiovascular function in whole animals, isolated myocardium and single cardiac cells. Current ongoing projects are (1) to elucidate the mechanisms, metabolic regulation, and therapeutic potential of cardiac regeneration using stem/progenitor cells from extra-cardiac sources, such as bone marrow, iPS and resident cardiac stem cells and (2) the molecular mechanisms regulating the development and progression of primary amyloid cardiomyopathy.

Cardiac Regeneration- Recent work has demonstrated that terminally-differentiated organs are continuously undergoing cellular turnover with differentiation of tissue-specific progenitor cells. Our laboratory has identified a specific subpopulation of progenitor cells within adult myocardium, characterized by a distinct Hoechst dye efflux pattern. Furthermore, we have shown that these progenitor cells are capable of differentiation into functional cardiomyocytes. Our current research focuses on understanding the specific signaling pathways that regulate cardiac stem cells proliferation and differentiation in the normal heart, as well as following injury, and developing approaches to manipulate and promote cardiac regeneration in-vivo.

Cardiac Amyloidosis- Our laboratory has been the first to report that immunoglobulin light chain proteins (amyloid precursors) directly provoke cellular toxicity in isolated cardiomyocytes and whole hearts. We recently identified key stress activated signaling pathways that are responsible for the light chain mediate cardiac toxicity and subsequent dysfunction. Our current research focuses on further elucidating these cellar processes and the mechanisms by which they result in the rapid onset of cardiac dysfunction and failure, with an ultimate goal of identifying new therapeutic targets for patients with primary amyloid cardiomyopathy.

Last Update: 8/22/2013


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