Senescence and apoptosis block hematopoietic activation of quiescent hematopoietic stem cells with short telomeres

Author:

Wang Jianwei12,Lu Xin3,Sakk Vadim4,Klein Christoph A.35,Rudolph Karl Lenhard12

Affiliation:

1. Leibniz Institute of Age Research, Fritz Lipmann Institute e.V., Jena, Germany;

2. Research Group on Molecular Aging, Faculty of Medicine, Friedrich-Schiller-University, Jena, Germany;

3. Experimental Medicine and Therapy Research, University Regensburg, Regensburg, Germany;

4. Cooperation Group: Leibniz Institute for Age Research and University Ulm, Ulm, Germany; and

5. Fraunhofer-Institut für Toxikologie und Experimentelle Medizin, Project Group Personalized Tumor Therapy, Regensburg, Germany

Abstract

Key Points DNA damage induced by telomere shortening resides in most quiescent HSCs. Senescence and apoptosis compromise the activation of HSCs with dysfunctional telomeres.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Reference21 articles.

1. Telomere shortening associated with disease evolution patterns in myelodysplastic syndromes.;Ohyashiki;Cancer Res,1994

2. Telomere maintenance and human bone marrow failure.;Calado;Blood,2008

3. Bone marrow failure and the new telomere diseases: practice and research.;Young;Hematology,2012

4. Telomere diseases.;Calado;N Engl J Med,2009

5. Telomeres, stem cells, and hematology.;Lansdorp;Blood,2008

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