JMJD3-mediated senescence is required to overcome stress-induced hematopoietic defects.

Yuichiro Nakata, Takeshi Ueda, Yasuyuki Sera, Miho Koizumi, Katsutoshi Imamura, Akinori Kanai, Ken-Ichiro Ikeda, Norimasa Yamasaki, Akiko Nagamachi, Kohei Kobatake, Masataka Taguchi, Yusuke Sotomaru, Tatsuo Ichinohe, Zen-Ichiro Honda, Takuro Nakamura, Ichiro Manabe, Toshio Suda, Keiyo Takubo, Osamu Kaminuma, Hiroaki Honda

Department of Systems Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan. [email protected] of Systems Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan. [email protected]. · pubmed

Paper

Abstract

Cellular senescence in stem cells compromises regenerative capacity, promotes chronic inflammation, and is implicated in aging. Hematopoietic stem and progenitor cells (HSPCs) are responsible for producing mature blood cells, however, how cellular senescence influences their function is largely unknown. Here, we show that JMJD3, a histone demethylase, activates cellular senescence by upregulating p16

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Research summary

JMJD3 activates cellular senescence in hematopoietic stem and progenitor cells by upregulating p16. This research addresses the mechanisms of cellular senescence, which is a fundamental aspect of aging and its impact on regenerative capacity, thus contributing to the understanding of aging processes.

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