Shu Fang Liu, PhD

Investigator, Pulmonary and Critical Care Medicine, The Feinstein Institute for Medical Research

Professor of Medicine, Hofstra Northwell School of Medicine

Phone: (516) 562-1305
Email: sliu@northwell.edu

About the Investigator

Dr. Shu Fang Liu graduated from Shanghai Second Medical University in China and received his PhD in Molecular Pharmacology from Imperial College, University of London, England. He is currently an investigator at the Feinstein Institute for Medical Research and professor of medicine at Hofstra Northwell School of Medicine. Dr. Liu has been investigating the molecular and cellular mechanisms of multiple organ injury caused by sepsis, a condition that claimed thousands of lives each year for 20 years.

Research Focus

Dr. Liu’s laboratory focuses on molecular mechanisms of septic shock, and septic multiple organ injury (MOI), conditions that claim thousands of life each year. Using modern molecular biology techniques, we are unveiling the molecular and cellular events that take place when bacterial infections initiate the inflammatory process and lead to the development of septic shock and septic MOI. Our goal is to discover the key molecules that can be new targets for developing new therapies for treating these life-threatening conditions. We have discovered that activation of endothelium, a monolayer of cells lining the inner surface of all our blood vessels, by inflammatory mediators is a “rate-limiting” factor determining the severity of organ injury. Prevention of endothelium activation and injury without blocking inflammation is sufficient to mitigate MOI caused by sepsis. We are currently developing strategies to strengthen the endothelium or to accelerate the repair of the injured endothelium. These studies will lead to the development of novel anti-sepsis therapies.

We have also discovered that in addition to triggering uncontrolled systemic inflammation, bacterial infection also suppresses the expression of multiple “housekeeping genes”, whose products are critical for the maintenance of normal organ functions, and impairs our body’s anti-inflammatory and protective mechanisms. We are investigating how bacterial infection represses housekeeping gene expression and impairs the anti-inflammatory and protective mechanisms, and are trying to find the ways of boost these anti-inflammatory mechanisms.

Lab Members

Xiaobing Ye
Phone: (516) 562-1604
Email: xye@nshs.edu

Education

Shanghai Second Medical University, China
Degree: BM
1977
Field of Study: Medicine

Wenzhou Medical College, China
Degree: MS
1982
Field of Study: Cardiovascular Diseases

Imperial College, University of London, England
Degree: PhD
1993
Field of Study: Molecular Pharmacology

National Heart & Lung Institute, University of London, England
Degree: Postdoctoral
1995
Field of Study: Molecular Pharmacology

Awards & Honors

1988 Scientific Achievement Award, Third Place, Zhejiang Province, China
1989 Scientific Achievement Award, First Place, Wenzhou City, Zhejiang, China
1990 Science and Technology Advance Award, NanShi Foundation, Hong Kong
1990 Predoctoral Fellowship, British Heart Foundation
1990 Overseas Research Student Award, British Council, United Kingdom
1991 Overseas Research Student Award, British Council, United Kingdom
1992 Overseas Research Student Award, British Council, United Kingdom
1992 Winner of Best Scientific Paper, Guanghua Foundation
1993 Postdoctoral Fellowship, British Heart Foundation
2013 Fellow, American Heart Association

Publications
  1. Fang, G, Song, D., Ye, X, Mao, S-Z, Liu, G, and Liu SF. “Chronic Intermittent Hypoxia Exposure Induces Atherosclerosis in ApoE Knockout Mice: Role of NF-κB p50.” Am J Pathol. 181:1530-9, 2012).
  2. Song, D, Fang, G, Mao, SZ, Ye, X, Liu, G, Gong, Y and Liu SF. “Chronic intermittent hypoxia induces atherosclerosis by NF-κB-dependent mechanisms.” Biochim Biophys Acta Mol Dis. 1822:1650-9, (2012).
  3. Xu, H, Ye, X, Steinberg, H and Liu SF. “Selective blockade of endothelial NF-kappaB pathway differentially affects systemic inflammation and multiple organ dysfunction and injury in septic mice.” J Pathol 220:490-498, 2010.
  4. Liu G, Ye X, Miller EJ, Liu SF. NF-κB-to-AP-1 switch: a mechanism regulating transition from endothelial barrier injury to repair in endotoxemic mice. Sci Rep. 2014 Jul 2;4:5543.
  5. Mao SZ, Ye X, Liu G, Song D, Liu SF. An Obligatory Role of NF-κB in Mediating Bone Marrow Derived Endothelial Progenitor Cell Recruitment and Proliferation Following Endotoxemic Multiple Organ Injury in Mice. PLoS One. 2014 Oct 21;9(10):e111087.
  6. Ye, X., Ding, D., Zhou, Z., Chen, G. and Liu, S.F. “Divergent roles of endothelial NF-κB in multiple organ injury and bacterial clearance in murine models of sepsis.” J. Exp. Med. 205:1303-1315 2008.

View more at PubMed