Ronglih Liao

Ronglih Liao studied hard as a teenager in Taiwan, but science was just one among many wide-ranging interests. At age 17, however, her focus abruptly became clear when her father was diagnosed with lung cancer, eventually leading Liao to a career in basic science with the potential to translate understanding into therapies for both rare and common cardiovascular diseases. After obtaining a chemistry degree, Liao fulfilled a promise to her late father to obtain an advanced degree overseas. For her PhD thesis at the University of Alabama Birmingham, she examined the interaction of troponin I with troponin C in bovine cardiac muscle. Then, Liao was recruited by 2 amazing mentors with independent laboratories and complementary expertise, Drs Judith Gwathmey and Joanne S. Ingwall, to undertake a collaborative project in cardiac physiology and myocardial energetics at Harvard Medical School. At the time, the concept that failing hearts were energy-starved was not yet accepted, and Liao deployed P nuclear magnetic resonance to detect decreased energy reserve in a model of dilated cardiomyopathy—baggy and sick turkey hearts—and establish its relationship to contractile performance. Liao set up her first independent laboratory at the Boston University School of Medicine, where she benefited from the university’s status as an internationally recognized center for the study of amyloidosis. Perfusing human immunoglobulin light chain proteins (amyloid precursors) into mouse heart, her laboratory was the first to demonstrate what the amyloidosis experts at Boston University had suspected—that amyloid light chain proteins were cardiotoxic and contributed directly to the pathogenesis and rapid progression of amyloid cardiomyopathy, independent of fibril formation and deposition. In 2005, Liao moved to Harvard Medical School, where she is now professor of medicine. At Brigham and Women’s Hospital, she directs the Cardiac Muscle Research Laboratory (since 2005), the Cardiovascular Flow Cytometry Core (since 2007), and the Cardiovascular Physiology Core (since 2010), aiming to bring innovative technologies to the cardiovascular research community. Liao continues her work on cardiac amyloidosis, identifying key stress-activated signaling pathways responsible for the light chain–mediated cardiac toxicity and subsequent dysfunction. Addressing the far-larger group of patients who may someday develop heart failure after myocardial infarction, Liao’s laboratory strives to understand the molecular mechanisms that mediate the transition from a normal to a failing heart. The laboratory identified a subpopulation of progenitor cells within adult myocardium that were capable of differentiation into functional cardiomyocytes. Her current research is focused on understanding the signaling pathways that regulate cardiac stem cell proliferation and differentiation in normal development, as well as after injury, and in developing approaches to manipulate and promote cardiac regeneration in vivo. In a recent article, the group revealed microRNA-34a to be a critical regulator of cardiac repair and regeneration in neonatal rodents after myocardial infarction, suggesting that modulation of miR-34a might be harnessed for cardiac repair in adult myocardium. In 2006, Liao became an editorial board member of Circulation Research, where she has published regularly since her first cardiac physiology paper was accepted there in 1993. She joined the American Heart Association’s Basic Cardiovascular Sciences Council in 1997, and begins a 2-year term as chair in July. In a recent interview, Liao discussed her background, her plans for the Council on Basic Cardiovascular Sciences (BCVS), and the goal she has held since she first became excited about science—to translate her work to somehow help patients.