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      Iron overload inhibits self‐renewal of human pluripotent stem cells via DNA damage and generation of reactive oxygen species

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          Iron overload affects the cell cycle of various cell types, but the effect of iron overload on human pluripotent stem cells has not yet been reported. Here, we show that the proliferation capacities of human embryonic stem cells (hESCs) and human induced pluripotent stem cells (hiPSCs) were significantly inhibited by ferric ammonium citrate (FAC) in a concentration‐dependent manner. In addition, deferoxamine protected hESCs/hiPSCs against FAC‐induced cell‐cycle arrest. However, iron overload did not affect pluripotency in hESCs/hiPSCs. Further, treatment of hiPSCs with FAC resulted in excess reactive oxygen species production and DNA damage. Collectively, our findings provide new insights into the role of iron homeostasis in the maintenance of self‐renewal in human pluripotent stem cells.


          We demonstrated in this study that iron overload could severely impair the proliferation of human embryonic stem cells/human induced pluripotent stem cells through excess reactive oxygen species production and DNA damage. These results imply a role of iron homeostasis in maintaining the self‐renewal of human embryonic stem cells/human induced pluripotent stem cells.

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          Stems cells and the pathways to aging and cancer.

          The aging of tissue-specific stem cell and progenitor cell compartments is believed to be central to the decline of tissue and organ integrity and function in the elderly. Here, we examine evidence linking stem cell dysfunction to the pathophysiological conditions accompanying aging, focusing on the mechanisms underlying stem cell decline and their contribution to disease pathogenesis.
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            Stem cells and the impact of ROS signaling.

            An appropriate balance between self-renewal and differentiation is crucial for stem cell function during both early development and tissue homeostasis throughout life. Recent evidence from both pluripotent embryonic and adult stem cell studies suggests that this balance is partly regulated by reactive oxygen species (ROS), which, in synchrony with metabolism, mediate the cellular redox state. In this Primer, we summarize what ROS are and how they are generated in the cell, as well as their downstream molecular targets. We then review recent findings that provide molecular insights into how ROS signaling can influence stem cell homeostasis and lineage commitment, and discuss the implications of this for reprogramming and stem cell ageing. We conclude that ROS signaling is an emerging key regulator of multiple stem cell populations.
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              Impact of genomic damage and ageing on stem cell function.

              Impairment of stem cell function contributes to the progressive deterioration of tissue maintenance and repair with ageing. Evidence is mounting that age-dependent accumulation of DNA damage in both stem cells and cells that comprise the stem cell microenvironment are partly responsible for stem cell dysfunction with ageing. Here, we review the impact of the various types of DNA damage that accumulate with ageing on stem cell functionality, as well as the development of cancer. We discuss DNA-damage-induced cell intrinsic and extrinsic alterations that influence these processes, and review recent advances in understanding systemic adjustments to DNA damage and how they affect stem cells.

                Author and article information

                FEBS Open Bio
                FEBS Open Bio
                FEBS Open Bio
                John Wiley and Sons Inc. (Hoboken )
                07 April 2020
                May 2020
                : 10
                : 5 ( doiID: 10.1002/feb4.v10.5 )
                : 726-733
                [ 1 ] Department of Pharmacy The Affiliated Second Hospital Harbin Medical University Harbin China
                [ 2 ] Department of Pharmacology (The Key Laboratory of Cardiovascular Research, Ministry of Education) College of Pharmacy Harbin Medical University Harbin China
                [ 3 ] Beijing Ruihua Heart Rehabilitation Research Center China
                [ 4 ] Department of Clinical Laboratory Fourth Affiliated Hospital of Harbin Medical University China
                Author notes
                [* ] Correspondence

                Y. Liu, Department of Clinical Laboratory at The Fourth Affiliated Hospital of Harbin Medical University, Yiyuan street 37, Harbin, 150001, China

                E‐mail: rainfall1982@ 123456163.com


                W. Ma, Department of Pharmacy at The Affiliated Second Hospital, Harbin Medical University, Xuefu Road 246, Harbin, 150081, China

                E‐mail: 787973558@ 123456qq.com

                © 2020 The Authors. Published by FEBS Press and John Wiley & Sons Ltd.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                Page count
                Figures: 4, Tables: 0, Pages: 8, Words: 3929
                Funded by: National Key R&D Program of China
                Award ID: 2017YFC1307403
                Funded by: National Natural Science Fund of China
                Award ID: 81573434
                Award ID: 81730012
                Funded by: Young Creative Talents Training Program of Heilongjiang Provincial Universities
                Award ID: UNPYSCT‐2015034
                Research Article
                Research Articles
                Custom metadata
                May 2020
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.1 mode:remove_FC converted:01.05.2020


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