Oxidative Stress, Bone Marrow Failure, and Genome Instability in Hematopoietic Stem Cells

International Journal of Molecular Sciences

Christine Richardson¹  Shan Yan²  C. Greer Vestal² 

[1] Department of Biological Sciences, UNC Charlotte, 9201 University City Blvd., Woodward Hall Room 386B, Charlotte, NC 28223, USA;

关键词: oxidative damage;    reactive oxygen species;    ROS;    bone marrow failure;    base excision repair;    excision repair cross complement;    aging;    genome stability;    cancer;   

DOI  :  10.3390/ijms16022366

来源: mdpi

【 摘 要 】

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.

【 授权许可】

CC BY   
© 2015 by the authors; licensee MDPI, Basel, Switzerland.