TY - JOUR
T1 - Reactive oxygen species and hematopoietic stem cell senescence
AU - Shao, Lijian
AU - Li, Hongliang
AU - Pazhanisamy, Senthil K.
AU - Meng, Aimin
AU - Wang, Yong
AU - Zhou, Daohong
N1 - Funding Information:
Acknowledgments This study was supported in part by grants from the National Institutes of Health (R01-CA086688, CA102558, and AI080421), and a grant from the National Natural Science Foundation of China (NSFC 30828011), the Winthrop Rockefeller Endowment for Leukemia Research, and the Arkansas Research Alliance Scholarship from the Arkansas Science & Technology Authority.
PY - 2011/7
Y1 - 2011/7
N2 - 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.
AB - 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.
KW - Hematopoietic stem cells
KW - NADPH oxidase
KW - Reactive oxygen species
KW - Senescence
KW - p16
KW - p38
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U2 - 10.1007/s12185-011-0872-1
DO - 10.1007/s12185-011-0872-1
M3 - Article
C2 - 21567162
AN - SCOPUS:79960077503
SN - 0925-5710
VL - 94
SP - 24
EP - 32
JO - International journal of hematology
JF - International journal of hematology
IS - 1
ER -