Reactive oxygen species and hematopoietic stem cell senescence

Lijian Shao, Hongliang Li, Senthil K. Pazhanisamy, Aimin Meng, Yong Wang, Daohong Zhou

Research output: Contribution to journalArticlepeer-review

150 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)24-32
Number of pages9
JournalInternational journal of hematology
Issue number1
StatePublished - Jul 2011
Externally publishedYes


  • Hematopoietic stem cells
  • NADPH oxidase
  • Reactive oxygen species
  • Senescence
  • p16
  • p38

ASJC Scopus subject areas

  • Hematology


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