Mitochondrial DNA Aberrations and Pathophysiological Implications in Hematopoietic Diseases, Chronic Inflammatory Diseases, and Cancers.
- Author:
Hye Ran KIM
1
;
Stephanie Jane WON
;
Claire FABIAN
;
Min Gu KANG
;
Michael SZARDENINGS
;
Myung Geun SHIN
Author Information
- Publication Type:Research Support, Non-U.S. Gov't ; Review
- Keywords: mtDNA; Aberrations; Diseases
- MeSH: DNA, Mitochondrial/*genetics/metabolism; Hematologic Diseases/genetics/*pathology; Humans; *Inflammation; Mitochondria/genetics; Mutation; Neoplasms/genetics/*pathology; Oxidative Stress; Reactive Oxygen Species/metabolism
- From:Annals of Laboratory Medicine 2015;35(1):1-14
- CountryRepublic of Korea
- Language:English
- 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.
