{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T00:46:19Z","timestamp":1792197979727,"version":"4.4.0"},"reference-count":175,"publisher":"SAGE Publications","issue":"9","license":[{"start":{"date-parts":[[2014,3,1]],"date-time":"2014-03-01T00:00:00Z","timestamp":1393632000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Antioxidants &amp; Redox Signaling"],"published-print":{"date-parts":[[2014,3]]},"abstract":"<jats:p>\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Significance:<\/jats:italic>\n                    <\/jats:bold>\n                    Exposure to ionizing radiation (IR) as the result of nuclear accidents or terrorist attacks is a significant threat and a major medical concern. Hematopoietic stem cell (HSC) injury is the primary cause of death after accidental or intentional exposure to a moderate or high dose of IR. Protecting HSCs from IR should be a primary goal in the development of novel medical countermeasures against radiation.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Recent Advances:<\/jats:italic>\n                    <\/jats:bold>\n                    Significant progress has been made in our understanding of the mechanisms by which IR causes HSC damage. The mechanisms include (i) induction of HSC apoptosis\n                    <jats:italic toggle=\"yes\">via<\/jats:italic>\n                    the p53-Puma pathway; (ii) promotion of HSC differentiation\n                    <jats:italic toggle=\"yes\">via<\/jats:italic>\n                    the activation of the G-CSF\/Stat3\/BATF-dependent differentiation checkpoint; (iii) induction of HSC senescence\n                    <jats:italic toggle=\"yes\">via<\/jats:italic>\n                    the ROS-p38 pathway; and (iv) damage to the HSC niche.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Critical Issues:<\/jats:italic>\n                    <\/jats:bold>\n                    Induction of apoptosis in HSCs and hematopoietic progenitor cells is primarily responsible for IR-induced acute bone marrow (BM) injury. Long-term BM suppression caused by IR is mainly attributable to the induction of HSC senescence. However, the promotion of HSC differentiation and damage to the HSC niche can contribute to both the acute and long-term effects of IR on the hematopoietic system.\n                    <jats:bold>\n                      <jats:italic toggle=\"yes\">Future Directions:<\/jats:italic>\n                    <\/jats:bold>\n                    In this review, we have summarized a number of recent findings that provide new insights into the mechanisms whereby IR damages HSCs. These findings will provide new opportunities for developing a mechanism-based strategy to prevent and\/or mitigate IR-induced BM suppression.\n                    <jats:italic toggle=\"yes\">Antioxid. Redox Signal.<\/jats:italic>\n                    20, 1447\u20131462.\n                  <\/jats:p>","DOI":"10.1089\/ars.2013.5635","type":"journal-article","created":{"date-parts":[[2013,10,14]],"date-time":"2013-10-14T08:32:27Z","timestamp":1381739547000},"page":"1447-1462","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":318,"title":["Hematopoietic Stem Cell Injury Induced by Ionizing Radiation"],"prefix":"10.1177","volume":"20","author":[{"given":"Lijian","family":"Shao","sequence":"first","affiliation":[{"name":"University of Arkansas for Medical Sciences"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi","family":"Luo","sequence":"additional","affiliation":[{"name":"University of Arkansas for Medical Sciences"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daohong","family":"Zhou","sequence":"additional","affiliation":[{"name":"University of Arkansas for Medical Sciences"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2014,3,20]]},"reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.stem.2010.09.013"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1205314"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2002-07-2334"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1038\/nm0403-369"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jvs.2010.06.012"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0092-8674(02)00697-9"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1196\/annals.1392.005"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2004.07.004"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1038\/nm973"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1667\/RR2220.1"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.canlet.2011.12.012"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2005.02.001"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1089\/scd.2004.13.548"},{"key":"e_1_3_2_15_2","doi-asserted-by":"publisher","DOI":"10.1093\/emboj\/cdg417"},{"key":"e_1_3_2_16_2","doi-asserted-by":"publisher","DOI":"10.1038\/197452a0"},{"key":"e_1_3_2_17_2","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00044.2005"},{"key":"e_1_3_2_18_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-0609.1989.tb00264.x"},{"key":"e_1_3_2_19_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood.V90.4.1345"},{"key":"e_1_3_2_20_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2005.02.003"},{"key":"e_1_3_2_21_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0531-5565(01)00160-7"},{"key":"e_1_3_2_22_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2011-06-361626"},{"key":"e_1_3_2_23_2","doi-asserted-by":"publisher","DOI":"10.1089\/152581602753658547"},{"key":"e_1_3_2_24_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20081297"},{"key":"e_1_3_2_25_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.176.10.5720"},{"key":"e_1_3_2_26_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20101688"},{"key":"e_1_3_2_27_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.261562798"},{"key":"e_1_3_2_28_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature05077"},{"key":"e_1_3_2_29_2","doi-asserted-by":"publisher","DOI":"10.1182\/blood-2006-05-022640"},{"key":"e_1_3_2_30_2","first-page":"159","article-title":"Apoptosis in bone marrow cells of mice with different p53 genotypes after gamma-rays irradiation in vitro","volume":"14","author":"Cui YF","year":"1995","unstructured":"Cui YF, , Zhou PK, , Woolford LB, , Lord BI, , Hendry JH, , and Wang DW. 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