{"title":"Midkine和TNFSF10作为I型干扰素的下游分子参与骨髓纤维化的治疗。","authors":"Yaoyao Chen, Fanxiang Yin, Xiaoqian Wang, Huilin Zhang, Ping Tang, Mengjiao Xue, Nannan Sun, Jin Li, Chang Chen, Bingjie Wang, Qingxuan Xin, Juanxia Zhou, Yingmei Li, Shuya Wang, Shaohua Yan, Jiani Li, Yunling Zhu, Bo Qin, Baohong Yue, Yong Jiang, Rongqun Guo","doi":"10.1016/j.bbagen.2025.130863","DOIUrl":null,"url":null,"abstract":"<p><p>Myelofibrosis (MF), a myeloproliferative neoplasm, remains incurable for most patients. Although some individuals are eligible for allogeneic hematopoietic stem cell transplantation, current therapies generally slow disease progression rather than achieve a cure. In this study, we found that type I interferon (IFN) treatment enhances midkine (MDK) expression, and MDK is involved in the differentiation and maturation of progenitor cells. Notably, MDK treatment drives tumor cells into the cell cycle, thereby increasing the therapeutic effect of busulfan. Furthermore, MDK promotes osteogenic differentiation of mesenchymal stem cells (MSC), contributing to the remodeling of the bone marrow microenvironment. In addition, type I IFN upregulates TNFSF10, leading to tumor cell death through mutual killing.</p>","PeriodicalId":8800,"journal":{"name":"Biochimica et biophysica acta. General subjects","volume":" ","pages":"130863"},"PeriodicalIF":2.2000,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Midkine and TNFSF10 as downstream molecules of type I interferon are involved in the treatment of myelofibrosis.\",\"authors\":\"Yaoyao Chen, Fanxiang Yin, Xiaoqian Wang, Huilin Zhang, Ping Tang, Mengjiao Xue, Nannan Sun, Jin Li, Chang Chen, Bingjie Wang, Qingxuan Xin, Juanxia Zhou, Yingmei Li, Shuya Wang, Shaohua Yan, Jiani Li, Yunling Zhu, Bo Qin, Baohong Yue, Yong Jiang, Rongqun Guo\",\"doi\":\"10.1016/j.bbagen.2025.130863\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Myelofibrosis (MF), a myeloproliferative neoplasm, remains incurable for most patients. Although some individuals are eligible for allogeneic hematopoietic stem cell transplantation, current therapies generally slow disease progression rather than achieve a cure. In this study, we found that type I interferon (IFN) treatment enhances midkine (MDK) expression, and MDK is involved in the differentiation and maturation of progenitor cells. Notably, MDK treatment drives tumor cells into the cell cycle, thereby increasing the therapeutic effect of busulfan. Furthermore, MDK promotes osteogenic differentiation of mesenchymal stem cells (MSC), contributing to the remodeling of the bone marrow microenvironment. In addition, type I IFN upregulates TNFSF10, leading to tumor cell death through mutual killing.</p>\",\"PeriodicalId\":8800,\"journal\":{\"name\":\"Biochimica et biophysica acta. General subjects\",\"volume\":\" \",\"pages\":\"130863\"},\"PeriodicalIF\":2.2000,\"publicationDate\":\"2025-09-29\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biochimica et biophysica acta. General subjects\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1016/j.bbagen.2025.130863\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochimica et biophysica acta. General subjects","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1016/j.bbagen.2025.130863","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
Midkine and TNFSF10 as downstream molecules of type I interferon are involved in the treatment of myelofibrosis.
Myelofibrosis (MF), a myeloproliferative neoplasm, remains incurable for most patients. Although some individuals are eligible for allogeneic hematopoietic stem cell transplantation, current therapies generally slow disease progression rather than achieve a cure. In this study, we found that type I interferon (IFN) treatment enhances midkine (MDK) expression, and MDK is involved in the differentiation and maturation of progenitor cells. Notably, MDK treatment drives tumor cells into the cell cycle, thereby increasing the therapeutic effect of busulfan. Furthermore, MDK promotes osteogenic differentiation of mesenchymal stem cells (MSC), contributing to the remodeling of the bone marrow microenvironment. In addition, type I IFN upregulates TNFSF10, leading to tumor cell death through mutual killing.
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