DEPARTMENT OF CARDIOVASCULAR MEDICINE KYUSHU UNIVERSITY GRADUATE SCHOOL OF MEDICAL SCIENCES

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Research Units

Heart Failure Research Unit

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menu Research Outline Main Research Themes and Relevant Publications Principle Investigator of the group Staff and Research Focus

Main Research Themes and Relevant Publications


  1. Mitochondrial DNA (mtDNA) damage and reactive oxygen species generation in heart failure
  2. Research related to the roles of mitochondrial transcription factor A (TFAM) in heart failure
  3. The mechanisms of anti-remodeling effects by vagal nerve stimulation

1. Mitochondrial DNA (mtDNA) damage and reactive oxygen species generation in heart failure



Vicious cycle of ROS generation and mtDNA damage in mitochondria

We have shown that reactive oxygen species are increased in the myocardium of heart failure, and also demonstrated the vicious cycle in which mtDNA damage causes dysfunction of the mitochondrial electron transfer system generating reactive oxygen species, which further damage mtDNA. At present we are expanding our studies on the control of mtDNA damage, which may potentially lead to the development of novel therapies for various chronic diseases including heart failure.

Relevant publications
  1. Ide T, Tsutsui H, Hayashidani S, Kang D, Suematsu N, Nakamura K, Utsumi H, Hamasaki N, Takeshita A. Mitochondrial DNA damage and dysfunction associated with oxidative stress in failing hearts after myocardial infarction. Circ Res. 2001 Mar 16;88(5):529-35.
  2. Tsutsui H, Ide T, Hayashidani S, Suematsu N, Shiomi T, Wen J, Nakamura Ki, Ichikawa K, Utsumi H, Takeshita A. Enhanced generation of reactive oxygen species in the limb skeletal muscles from a murine infarct model of heart failure. Circulation. 2001 Jul 10;104(2):134-6.
  3. Tsutsui H, Ide T, Shiomi T, Kang D, Hayashidani S, Suematsu N, Wen J, Utsumi H, Hamasaki N, Takeshita A. 8-oxo-dGTPase, which prevents oxidative stress-induced DNA damage, increases in the mitochondria from failing hearts. Circulation. 2001 Dec 11;104(24):2883-5.
  4. Kinugawa S, Tsutsui H, Satoh S, Takahashi M, Ide T, IgarashiSaito K, Arimura K, Egashira K, Takeshita A. Role of Ca2+ availability to myofilaments and their sensitivity to Ca2+ in myocyte contractile dysfunction in heart failure. Cardiovasc Res. 1999 Nov;44(2):398-406.
  5. Ide T, Tsutsui H, Kinugawa S, Suematsu N, Hayashidani S, Ichikawa K, Utsumi H, Machida Y, Egashira K, Takeshita A. Direct evidence for increased hydroxyl radicals originating from superoxide in the failing myocardium. Circ Res. 2000 Feb 4;86(2):152-7.

  1. Mitochondrial DNA (mtDNA) damage and reactive oxygen species generation in heart failure
  2. Research related to the roles of mitochondrial transcription factor A (TFAM) in heart failure
  3. The mechanisms of anti-remodeling effects by vagal nerve stimulation

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