Progress in Hematology Hematopoietic stem cell aging

International Journal of Hematology

, Volume 94, Issue 1, pp 24-32

First online:

Reactive oxygen species and hematopoietic stem cell senescence

  • Lijian ShaoAffiliated withDivision of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences
  • , Hongliang LiAffiliated withDivision of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical SciencesDepartment of Biochemistry and Molecular Biology, Institute of Radiation Medicine, Chinese Academy of Medical Sciences
  • , Senthil K. PazhanisamyAffiliated withDivision of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical Sciences
  • , Aimin MengAffiliated withDepartment of Biochemistry and Molecular Biology, Institute of Radiation Medicine, Chinese Academy of Medical Sciences
  • , Yong WangAffiliated withDepartment of Pathology, Medical University of South Carolina
  • , Daohong ZhouAffiliated withDivision of Radiation Health, Department of Pharmaceutical Sciences, University of Arkansas for Medical SciencesWinthrop P. Rockefeller Cancer Institute, University of Arkansas for Medical Sciences Email author 

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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)-p16Ink4a (p16) pathway in mediating ROS-induced HSC senescence.

Keywords

Reactive oxygen species Hematopoietic stem cells NADPH oxidase p38 p16 Senescence