title: Reactive oxygen species and hematopoietic stem cell senescence.
abstract: Hematopoietic stem cells (HSCs) are responsible for sustaining hematopoietic homeostasis and regeneration after injury for the entire lifespan of an organism through self-renewal, proliferation, differentiation, and mobilization. Their functions can be affected by reactive oxygen species (ROS) that are produced endogenously through cellular metabolism or after exposure to exogenous stress. At physiological levels, ROS function as signal molecules which can regulate a variety of cellular functions, including HSC proliferation, differentiation, and mobilization. However, an abnormal increase in ROS production occurs under various pathological conditions, which can inhibit HSC self-renewal and induce HSC senescence, resulting in premature exhaustion of HSCs and hematopoietic dysfunction. This review aims to provide a summary of a number of recent findings regarding the cellular sources of ROS in HSCs and the mechanisms of action whereby ROS induce HSC senescence. In particular, we highlight the roles of the p38 mitogen-activated protein kinase (p38)-p16(Ink4a) (p16) pathway in mediating ROS-induced HSC senescence.
authors.affiliation: Division of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
authors.forename: Lijian
authors.initials: L
authors.lastname: Shao
authors.affiliation: Division of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, AR, USA.|Department of Biochemistry and Molecular Biology, Institute of Radiation Medicine, Chinese Academy of Medical Sciences, Tianjin, China.
authors.forename: Hongliang
authors.initials: H
authors.lastname: Li
authors.affiliation: Division of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, AR, USA.
authors.forename: Senthil K
authors.initials: SK
authors.lastname: Pazhanisamy
authors.affiliation: Department of Biochemistry and Molecular Biology, Institute of Radiation Medicine, Chinese Academy of Medical Sciences, Tianjin, China.
authors.forename: Aimin
authors.initials: A
authors.lastname: Meng
authors.affiliation: Department of Pathology, Medical University of South Carolina, Charleston, SC, USA.
authors.forename: Yong
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Division of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences, Little Rock, AR, USA. dzhou@uams.edu.|Winthrop P. Rockefeller Cancer Institute, University of Arkansas for Medical Sciences, 4301 W Markham, #607, Little Rock, AR, 72205, USA. dzhou@uams.edu.
authors.forename: Daohong
authors.initials: D
authors.lastname: Zhou
mesh_terms: D016922:Cellular Senescence; D019941:Cyclin-Dependent Kinase Inhibitor p16; D006412:Hematopoietic Stem Cells / Q000502:physiology*; D006801:Humans; D017382:Reactive Oxygen Species; D015398:Signal Transduction; D048051:p38 Mitogen-Activated Protein Kinases
chemical_list: D019941:Cyclin-Dependent Kinase Inhibitor p16; D017382:Reactive Oxygen Species; D048051:p38 Mitogen-Activated Protein Kinases