Next Article in Journal
Quantitative Expression Analysis of APP Pathway and Tau Phosphorylation-Related Genes in the ICV STZ-Induced Non-Human Primate Model of Sporadic Alzheimer’s Disease
Next Article in Special Issue
Autophagy in DNA Damage Response
Previous Article in Journal
Antiproliferative and Antioxidant Properties of Anthocyanin Rich Extracts from Blueberry and Blackcurrant Juice
Previous Article in Special Issue
Potential Relationship between Inadequate Response to DNA Damage and Development of Myelodysplastic Syndrome
Article Menu
Issue 2 (February) cover image

Export Article

Open AccessReview
Int. J. Mol. Sci. 2015, 16(2), 2366-2385; doi:10.3390/ijms16022366

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

Department of Biological Sciences, UNC Charlotte, 9201 University City Blvd., Woodward Hall Room 386B, Charlotte, NC 28223, USA
*
Author to whom correspondence should be addressed.
Academic Editor: Guillermo T. Sáez
Received: 19 December 2014 / Revised: 6 January 2015 / Accepted: 16 January 2015 / Published: 22 January 2015
(This article belongs to the Special Issue DNA Damage and Repair in Degenerative Diseases 2014)
View Full-Text   |   Download PDF [1223 KB, uploaded 22 January 2015]   |  

Abstract

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. View Full-Text
Keywords: oxidative damage; reactive oxygen species; ROS; bone marrow failure; base excision repair; excision repair cross complement; aging; genome stability; cancer oxidative damage; reactive oxygen species; ROS; bone marrow failure; base excision repair; excision repair cross complement; aging; genome stability; cancer
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Richardson, C.; Yan, S.; Vestal, C.G. Oxidative Stress, Bone Marrow Failure, and Genome Instability in Hematopoietic Stem Cells. Int. J. Mol. Sci. 2015, 16, 2366-2385.

Show more citation formats Show less citations formats

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top