Reactive oxygen species (ROS) can be generated by defective endogenous reduction of oxygen by cellular enzymes or in the mitochondrial respiratory pathway, as well as by exogenous exposure to UV or environmental damaging agents. Regulation of intracellular ROS levels is critical since increases above normal concentrations lead to oxidative stress and DNA damage. A growing body of evidence indicates that the inability to regulate high levels of ROS leading to alteration of cellular homeostasis or defective repair of ROS-induced damage lies at the root of diseases characterized by both neurodegeneration and bone marrow failure as well as cancer. That these diseases may be reflective of the dynamic ability of cells to respond to ROS through developmental stages and aging lies in the similarities between phenotypes at the cellular level. This review summarizes work linking the ability to regulate intracellular ROS to the hematopoietic stem cell phenotype, aging, and disease.
Oxidative Stress, Bone Marrow Failure, and Genome Instability in Hematopoietic Stem Cells
C. Richardson,Shan Yan,C. G. Vestal
Published 2015 in International Journal of Molecular Sciences
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- Publication year
2015
- Venue
International Journal of Molecular Sciences
- Publication date
2015-01-22
- Fields of study
Biology, Medicine, Environmental Science
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- Source metadata
Semantic Scholar, PubMed
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