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Professor Kinya Otsu MD PhD

BHF Professor of Cardiology 

Otsu,KinyaThe James Black Centre
125 Coldharbour Lane
London SE5 9NU


Professor Kinya Otsu graduated from Osaka University Medical School, Japan and received his MD in 1983. Following two years training in residency in Internal Medicine, he began his career in cardiovascular research at the National Institute of Health, USA (1984-1988) followed by the University of Toronto, Canada (1988-1991) and University of Nice, France (1991). Professor Otsu moved back to Japan as a Senior Resident in Cardiology at the Osaka University Hospital. He was appointed as Assistant Professor in 1997 and subsequently as Associate Professor of Cardiology in 2005 at the Osaka University Graduate School of Medicine. In 2012, he was recruited from Osaka to London as Professor of Cardiology at King's College London and became a BHF Chair of Cardiology. (Photograph; courtesy of BHF)

Research interests

Our group aims to integrate physiological, biochemical, cell biological, molecular and genetic approaches to study the pathogenesis of heart failure. Cardiomyocyte death plays an important role in the progression of cardiacremodelling.  Neurohumoral factors and cytokinesthat are induced by mechanical stress on cardiomyocytes activatevarious intracellular signalling pathways, which regulate cell death. Our long term goal is to delineate the downstream mechanisms whereby activation of neurohumoral factors and cytokines mediate cardiomyocyte death and cardiac pathogenesis and to identify new therapeutic targets to treat patients with heart failure.  In addition, it is an important question how cytokines are produced. Three types of cell death, namely apoptosis, necrosis and autophagic death, have been reported. We have worked on the roles of each of these types of cardiomyocyte death in the pathogenesis of heart failure.

The group’s work involves the complementary use of a variety of techniques such as genetic engineering including target construction and ES cell manipulation, establishment of disease models (pressure-overloaded heart failure, myocardial infarction, ischemia/reperfusion injury), hemodynamic analysis, echocardiography, immunohistochemistry, histology, confocal microscopy, electronmicroscopy, adult and neonatal cardiomyocyte isolation, cell culture, biochemical assays, DNA cloning and expression.


Recent research accomplishments
We have initially identified a novel intracellular signal transduction pathway in vitro, in which neurohumoral factors and cytokines activate a Pyk2-Rac1-reactive oxygen species-apoptosis signal regulating kinase 1 (ASK1)-p38/JNK-NF-kB signalling pathway. Then, we have identified the in vivo role of each of the molecules in the above signal transduction pathway, using a broad range of novel genetically modified models. Our results show that ASK1-JNK is involved in apoptosis, whereas p38 and NF-kB protect cells from stress. The balance between the two signalling pathways will determine cell fate.

Turning to necrosis, we made the significant finding that the mitochondria permeability transition pore is the responsible molecule to execute cardiomyocyte necrosis. When necrosis is adequately controlled, it is possible to avoid necrotic cardiomyocyte death in ischemia-reperfusion injury,

We then investigated the role of autophagy. We found that autophagy does not contribute to cardiomyocyte cell death during stress but is instead a mechanism to protect cells against lethal stress by maintaining the quality of proteins and organelles. In addition, we found that autophagy is necessary to prevent inflammatory responses in failing hearts.


Current and future research directions
The role of necrosis in the development of heart failure remains to be elucidated, although necrosis is a very important form of cell death. A major focus of our work is to identify in detail the entire mechanism of cardiomyocyte necrosis and elucidate its role in heart failure. In order to control necrosis or autophagy, we also aim to identify the upstream and downstream signalling transduction mechanisms regulating both these processes.

During our autophagy research, we realized the importance of “degradation systems” in the pathogenesis of heart failure. Cell fate is determined by balance between “synthesis” and “degradation”. However, the latter has been paid much less attention compared to the former. We therefore aim to elucidate the role of degradation of proteins, DNA, RNA and organelles such as mitochondria in the genesis of heart failure.


Group members

Research Fellow/Associate

  • Dr Shigemiki Omiya
  • Dr Tomokazu Murakawa
  • Dr Jumpei Ito
  • Dr Yohei Tanada
  • Dr Mara-Camelia Rusu
  • Dr Javier Moncayo Arlandi
  • Dr Hajime Abe

Research Technician

  • Dr Saki Nakagawa
  • Dr Darran Hardy

 Professor Otsu's PA

  • Ms Andrea Kues-Johnson


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