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Mitochondrial DNA Aberrations and Pathophysiological Implications in Hematopoietic Diseases, Chronic Inflammatory Diseases, and Cancers

  • Kim, Hye-Ran (Department of Laboratory Medicine, Chonnam National University Medical School and Chonnam National University Hwasun Hospital) ;
  • Won, Stephanie Jane (Department of Integrative Biology, University of California) ;
  • Fabian, Claire (Department of Cell Therapy, Fraunhofer Institute for Cell Therapy and Immunology) ;
  • Kang, Min-Gu (Department of Laboratory Medicine, Chonnam National University Medical School and Chonnam National University Hwasun Hospital) ;
  • Szardenings, Michael (Department of Cell Therapy, Fraunhofer Institute for Cell Therapy and Immunology) ;
  • Shin, Myung-Geun (Department of Laboratory Medicine, Chonnam National University Medical School and Chonnam National University Hwasun Hospital)
  • Received : 2014.07.04
  • Accepted : 2014.11.11
  • Published : 2015.01.02

Abstract

Mitochondria are important intracellular organelles that produce energy for cellular development, differentiation, and growth. Mitochondrial DNA (mtDNA) presents a 10- to 20-fold higher susceptibility to genetic mutations owing to the lack of introns and histone proteins. The mtDNA repair system is relatively inefficient, rendering it vulnerable to reactive oxygen species (ROS) produced during ATP synthesis within the mitochondria, which can then target the mtDNA. Under conditions of chronic inflammation and excess stress, increased ROS production can overwhelm the antioxidant system, resulting in mtDNA damage. This paper reviews recent literature describing the pathophysiological implications of oxidative stress, mitochondrial dysfunction, and mitochondrial genome aberrations in aging hematopoietic stem cells, bone marrow failure syndromes, hematological malignancies, solid organ cancers, chronic inflammatory diseases, and other diseases caused by exposure to environmental hazards.

Keywords

Acknowledgement

Supported by : National Research Foundation of Korea (NRF)

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