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Kiichiro Yano, PhD

Instructor of Medicine
Beth Israel Deaconess Medical Center
Harvard Medical School

330 Brookline Avenue, RN 280B
Boston, MA 02215

Office: 617-667-2572
Fax: 617-667-2913
Email: kyano@bidmc.harvard.edu

Education/Training/Appointments

Kiichiro Yano received a Ph.D. in Molecular Biology from Hiroshima University, Higashi-Hiroshima, Japan in 2003. He then performed a post-doctoral study on the elucidation of molecular mechanisms in sepsis at Division of Molecular and Vascular Medicine at Beth Israel Deaconess Medical Center with Dr. William C Aird. In October 2008, Dr. Yano joined the Department of Emergency Medicine at Beth Israel Deaconess Medical Center and will continue his mechanistic investigations focusd on the role of the endothelium in critical illness including pneumonia, sepsis and hemorrhagic shock.

Research Interests

Endothelium Dysfunction in Inflammatory Diseases

Basic Research

My laboratory hypothesizes that endothelium plays a critical role in patho-physiology during sepsis. We are currently investigating the molecular mechanisms in vascular patho-physiology of sepsis using genetically modified mice and adenoviral technology in vivo and vitro. The aims of our study are i) to find pro- or anti-angiogenic mediators that impact on sepsis phenotype (mortality and morbidity), ii) to characterize the biological functions (molecular mechanisms) of those mediators, and iii) to explore the therapeutic and diagnostic potential of target mediators in sepsis. Our work requires extensive use of in vivo techniques such as animal surgeries, and wide spectrum of molecular techniques such as immunohistochemistry and in situ hybridization, isRNA and microRNA technologies.

VEGF and PlGF Axis During Sepsis

We previously demonstrated that elevated levels of VEGF during sepsis, and importantly that systemic blockade of VEGF, attenuated sepsis morbidity and mortality. These finding suggests that endothelium plays an important role in the patho-physiology of sepsis. Interestingly, we also found a protective effect of PlGF on sepsis-mediated morbidity and mortality. Since both VEGF and PlGF bind to VEGFR1, we have currently investigated the mechanism by which how VEGF and PlGF signaling is regulated during sepsis.

Other Diseases-Pneumonia and Hemorrhagic Shock

We are also investigating the importance of endothelium in pneumonia and hemorrhagic shock.

New and Noteworthy Publications

View all publications via PubMed >>

  1. Yano K, Okada Y, Beldi G, Shih SC, Bodyak N, Kang PM, Robson S, Luscinskas FW, Carmeliet P, Karumanchi SA, Aird WC. (2008) Elevated levels of placental growth factor represent an adaptive host response in sepsis. J. Exp. Med.,In Press. This study describes elevated levels of PlGF during sepsis protects against sepsis, at least in part, through the inhibition of VEGF signaling during sepsis.

  2. Shapiro N, Yano K, Okada H, Fisher C, Howell M, Spokes K, Ngo L, Anguc D, Aird WC. (2007). A prospective, observational study of soluble FLT-1 and vascular endothelial growth factor (VEGF) in sepsis. Shock, April; 29 (4): p452. This study describes elevated levels of circulating VEGF and sFlt-1 in septic patients. In particular sFlt-1 would be useful diagnostic marker for severity of sepsis.

  3. Yano K, Liaw PC, Mullington JM, Shih SC, Okada H, Bodyal N, Kang PM, Toltl L, Belikoff B, Buras J, Simms BT, Mizgard JP, Carmeliet P, Karumanchi SA, Aird WC. (2006) Vascular endothelial growth factor is an important detaminant of sepsis morbidity and mortality. J. Exp. Med., Jun 12: 203(6) p1447. This study describes, for the first time, that endothelium plays a critical role in patho-physiology of sepsis, and that systemic blockade of VEGF attenuates sepsis morbidity and mortality.

Contact Information

Nicole Magner, Administrative Assistant
Center for Vascular Biology Research
Beth Israel Deaconess Medical Center
Research North
99 Brookline Avenue
Boston, MA 02215
617-667-0654
info.cvbr@bidmc.harvard.edu