切换至 "中华医学电子期刊资源库"

中华细胞与干细胞杂志(电子版) ›› 2026, Vol. 16 ›› Issue (02) : 110 -118. doi: 10.3877/cma.j.issn.2095-1221.2026.02.006

综述

间充质干细胞治疗糖尿病肾病的研究进展
贾斐然, 司树涵, 张晓羽, 徐晓华()   
  1. 130033 长春,吉林大学中日联谊医院肾内科
  • 收稿日期:2025-09-04 出版日期:2026-04-01
  • 通信作者: 徐晓华
  • 基金资助:
    吉林省科技发展计划项目(20220204032YY)

Advances in the mesenchymal stem cell therapy for diabetic nephropathy

Feiran Jia, Shuhan Si, Xiaoyu Zhang, Xiaohua Xu()   

  1. Department of Nephrology, China-Japan Union Hospital, Jilin University, Changchun 130033, China
  • Received:2025-09-04 Published:2026-04-01
  • Corresponding author: Xiaohua Xu
引用本文:

贾斐然, 司树涵, 张晓羽, 徐晓华. 间充质干细胞治疗糖尿病肾病的研究进展[J/OL]. 中华细胞与干细胞杂志(电子版), 2026, 16(02): 110-118.

Feiran Jia, Shuhan Si, Xiaoyu Zhang, Xiaohua Xu. Advances in the mesenchymal stem cell therapy for diabetic nephropathy[J/OL]. Chinese Journal of Cell and Stem Cell(Electronic Edition), 2026, 16(02): 110-118.

糖尿病肾病(DN)是糖尿病最常见的微血管并发症,也是终末期肾病的主要诱因,主要由高糖环境引发的细胞损伤、炎症免疫紊乱、肾纤维化及血管破坏等复杂机制导致。传统治疗虽能延缓病情进展,但难以有效阻断肾脏损伤的不可逆恶化,探寻切实有效的治疗方法是亟待解决的关键问题。间充质干细胞(MSCs)及其外泌体因其自我更新能力与多向分化潜能,近年来成为DN治疗的研究热点。临床前研究表明,MSCs可通过包括细胞保护、调节炎症与免疫反应、抑制纤维化、表观遗传调控及"肠道—肾脏"调控等多种机制展现出修复肾脏结构与功能的潜力。不同注射途径(如静脉注射、肾动脉注射和局部注射)均显示出显著疗效。尽管如此,目前临床研究尚处于初步阶段,仅有小规模试验和病例报告表明MSCs具有一定肾脏保护潜力,其长期安全性、标准化治疗方案及不同来源MSCs的效能差异仍需进一步研究和验证。

Diabetic nephropathy (DN) is the most common microvascular complications of diabetes and serves as a leading cause of end-stage renal disease, which is caused by complex mechanisms, including cellular damage induced by hyperglycemia, dysregulated inflammatory and immune responses, renal fibrosis, and vascular injury. Although conventional treatments can delay the progress of the disease, they often fail to effectively halt the irreversible deterioration of renal function. Consequently, exploring practical and effective therapeutic strategies is a key issue that needs to be urgently addressed. In recent years, mesenchymal stem cells (MSCs) and their exosomes have garnered significant research interest due to their capacities for self-renewal and multi-lineage differentiation. Preclinical studies indicate that MSCs exhibit potential in restoring renal structure and function through various mechanisms, such as cytoprotection, modulation of inflammation and immune responses, inhibition of fibrosis, epigenetic regulation, and regulation of the gut–kidney axis. Multiple administration routes, including intravenous, renal arterial, and local injection, have demonstrated considerable therapeutic efficacy. Nonetheless, clinical research remains in the nascent stages, with only small-scale trials and case reports indicating that the MSCs have certain potential for renal protection. Their long-term safety, standardized treatment regimens, and the efficacy differences among MSCs from different sources still require further research and verification.

图1 间充质干细胞治疗糖尿病肾病的机制(CDR绘制)注:MSCs为间充质干细胞;MSCs-Exos为间充质干细胞外泌体;M1、M2为巨噬细胞表型;ROS为活性氧
图2 肾纤维化和间充质干细胞治疗肾纤维化的机制(CDR绘制)注:TGF-β为转化生长因子-β;TGF-β RⅠ为转化生长因子-β受体Ⅰ;TGF-β RⅡ为转化生长因子-β受体Ⅱ;MSCs为间充质干细胞;MSCs-Exos为间充质干细胞外泌体;ECM为细胞外基质;P为磷酸;α-SMA为α-平滑肌肌动蛋白
表1 间充质干细胞治疗DN的临床前研究总结
动物模型 造模方式 MSCs类型 注射方式 研究结论 参考文献
雄性C57BL/6小鼠 STZ诱导 hUCMSCs 静脉注射 通过降低血清中TNF-α的水平,减轻肾脏的炎症损伤 He等[7]
雄性SD大鼠 STZ诱导 hUCMSCs 静脉注射 通过激活Nrf2信号通路减少氧化损伤 Nie等[11]
雄性C57BL/6小鼠 高糖诱导 MSCs 静脉注射 通过下调NOX4表达抑制氧化应激通路激活 冯淑琪等[12]
雄性C57BL/6小鼠 STZ诱导 MSCs 静脉注射 通过隧道纳米管等途径向受损巨噬细胞转移线粒体 Barutta等[14]
雄性C57BL/6小鼠 STZ诱导 BMSCs 静脉注射 激活PGC-1α信号通路,促进线粒体生物发生,同时上调转录因子TFEB表达,改善溶酶体功能与自噬,加速受损线粒体清除 Yuan等[15]
雄性SD大鼠 高脂联合STZ诱导 hUCMSCs-Exos 静脉注射 抑制THBS1-CD36/CD47信号通路并调节肾组织中凋亡蛋白的表达,降低肾脏细胞凋亡水平 单云洁等[17]
雄性SD大鼠 STZ诱导 PMSCs 静脉注射 上调足细胞内的自噬相关蛋白(Beclin1和LC3)及SITR1和FOXO1表达水平,增强自噬活性 Liu等[20]
雄性C57BL/6小鼠 STZ诱导 hUCMSCs 静脉注射 通过降低血清中IL-6的水平,减轻肾脏的炎症损伤 Hsiao等[25]
雄性db/db小鼠 瘦素受体缺陷诱导 hUCMSCs-Exos 静脉注射 通过靶向调控NLRP3炎症小体信号通路抑制IL-18表达,减轻肾脏的炎症损伤 Wang等[27]
雄性C57BL/6小鼠 STZ诱导 MSCs-Exos 静脉注射 通过抑制NOD2信号通路的激活,对IL-18的表达水平及生物活性产生抑制作用 Wang等[28]
雄性CD1小鼠 STZ诱导 hUCMSCs 静脉注射 通过诱导巨噬细胞中Arg1表达,抑制M1型巨噬细胞的活化和浸润 Lee等[32]
雄性C57BL/6小鼠 STZ诱导 hUCMSCs-Exos 静脉注射 通过靶向抑制PI3KR1,解除其对PI3K/AKT通路的抑制,促进巨噬细胞极化成为具有抗炎和组织修复功能的M2型 Su等[33]
雄性SD大鼠 STZ诱导 BMSCs 静脉注射 通过减少肾脏中CD103+ DCs的数量、降低炎症因子表达并抑制CD8+ T细胞浸润,抑制树突状细胞介导的CD8+ T细胞反应 Zhang等[35]
雄性SD大鼠 STZ诱导 KMSCs 静脉注射 通过抑制TGF-β/Smad信号通路、调节miR-29a和miR-192的表达,减轻肾脏纤维化 Rafiee等[41]
雄性C57BL/6小鼠 STZ诱导 hUCMSCs-Exos 静脉注射 通过携带miR-125b-5p与SMO mRNA靶向结合,抑制SMO表达及Hedgehog信号通路激活,减少细胞外基质异常沉积 Zhang等[44]
雄性SD大鼠 STZ诱导 ADMSCs-Exos 静脉注射 通过靶向结合HDAC1的3'非编码区并抑制其表达,进而下调ET-1,抑制肾小球系膜细胞异常增殖、减轻肾纤维化与炎症反应 Hao等[47]
雄性C57BL/6小鼠 STZ诱导 BMSCs 静脉注射 通过调控Smad2/3/WTAP/m6A/ENO1信号轴,减轻肾皮质近曲小管上皮细胞损伤及肾脏病理损伤 Bai等[48]
雄性db/db小鼠 瘦素受体缺陷诱导 hUCMSCs-Exos 静脉注射 通过抑制Smad2/3磷酸化与核移位,下调METTL3水平,减少S1PR1的m6A修饰并恢复其表达,进一步增加S1PR1与铁死亡抑制蛋白结合,协同拮抗肾脏细胞的铁死亡 Huang等[49]
雄性SD大鼠 STZ诱导 hUCMSCs 静脉注射 通过归巢至结肠组织,上调肠道紧密连接蛋白的表达,阻止肠源性毒素进入血液循环,修复肠道屏障功能;同时重塑肠道菌群结构,提升有益菌菌群丰度,增加SCFAs的产生,激活肾脏对应受体,抑制肾脏局部氧化应激和炎症反应 Wu等[50]
雄性C57BL/6小鼠 STZ诱导 hUCMSCs-Exos 静脉注射 通过恢复DN状态下小鼠肠道内Prevotella的丰度,有效促进外周CD4+ Treg细胞的诱导与活化,改善肾脏损伤 Wang等[51]
雄性SD大鼠 STZ诱导 hUCMSCs 肾动脉注射 通过减少炎症、氧化应激和线粒体损伤等减少尿蛋白,保护肾功能 Yue等[52]
雄性SDT脂肪大鼠 肾切除+高盐饮水诱导 ADMSCs 局部注射 通过减少炎症反应、抑制蛋白尿保护足细胞和小管上皮细胞 Takemura等[53]
1
Kidney Disease:Improving Global Outcomes (KDIGO) Diabetes Work Group. KDIGO 2022 clinical practice guideline for diabetes management in chronic kidney disease[J]. Kidney Int, 2022, 102(5S): S1-S127.
2
He Y, Wang X, Wu Y, et al. Three decades of CKD due to diabetes mellitus type 2 in China, with projections of disease burden from 2022 to 2036: a systematic analysis for the Global Burden of Disease Study 2021[J]. Clin Kidney J, 2025, 18(10):sfaf265.
3
Zhang XX, Kong J, Yun K. Prevalence of diabetic nephropathy among patients with type 2 diabetes mellitus in China: a meta-analysis of observational studies[J]. J Diabetes Res, 2020, 2020:2315607.
4
Hamza AH, Al-Bishri WM, Damiati LA, et al. Mesenchymal stem cells: a future experimental exploration for recession of diabetic nephropathy[J]. Ren Fail, 2017, 39(1):67-76.
5
Hickson LJ, Herrmann SM, McNicholas BA, et al. Progress toward the clinical application of mesenchymal stromal cells and other disease-modulating regenerative therapies: examples from the field of nephrology[J]. Kidney360, 2021, 2(3):542-557.
6
Li X, Gao L, Li X, et al. Autophagy, pyroptosis and ferroptosis are rising stars in the pathogenesis of diabetic nephropathy[J]. Diabetes Metab Syndr Obes, 2024, 17:1289-1299.
7
He J, Liu B, Du X, et al. Amelioration of diabetic nephropathy in mice by a single intravenous injection of human mesenchymal stromal cells at early and later disease stages is associated with restoration of autophagy[J]. Stem Cell Res Ther, 2024, 15(1):66.
8
Zhang A, Fang H, Chen J, et al. Role of VEGF-A and LRG1 in abnormal angiogenesis associated with diabetic nephropathy[J]. Front Physiol, 2020, 11:1064.
9
Dwivedi S, Sikarwar MS. Diabetic nephropathy: Pathogenesis, mechanisms, and therapeutic strategies[J].Horm Metab Res, 2025, 57(1):7-17.
10
Sávio-Silva C, Soinski-Sousa PE, Simplício-Filho A, et al. Therapeutic potential of mesenchymal stem cells in a pre-clinical model of diabetic kidney disease and obesity[J]. Int J Mol Sci, 2021, 22(4):1546.
11
Nie P, Bai X, Lou Y, et al.Human umbilical cord mesenchymal stem cells reduce oxidative damage and apoptosis in diabetic nephropathy by activating Nrf2[J]. Stem Cell Res Ther, 2021, 12(1):450.
12
冯淑琪,金国荣,薛群航,等. 间充质干细胞影响NADHP氧化酶4抑制氧化应激通路治疗2型糖尿病肾病[J].中国生物化学与分子生物学报, 2025, 41(5):730-740
13
Zhao M, Liu S, Wang C, et al.Mesenchymal stem cell-derived extracellular vesicles attenuate mitochondrial damage and inflammation by stabilizing mitochondrial DNA[J]. ACS Nano, 2021, 15(1):1519-1538.
14
Barutta F, Corbetta B, Bellini S, et al. Protective effect of mesenchymal stromal cells in diabetic nephropathy: the in vitro and in vivo role of the M-Sec-tunneling nanotubes[J]. Clin Sci (Lond), 2024, 138(23):1537-1559.
15
Yuan Y, Yuan L, Li L, et al. Mitochondrial transfer from mesenchymal stem cells to macrophages restricts inflammation and alleviates kidney injury in diabetic nephropathy mice via PGC-1α activation[J]. Stem Cells, 2021, 39(7):913-928.
16
Chen L, Xiang E, Li C, et al. Umbilical cord-derived mesenchymal stem cells ameliorate nephrocyte injury and proteinuria in a diabetic nephropathy rat model[J]. J Diabetes Res, 2020, 2020:8035853.
17
单云洁, 于洋, 尹思琪, 等. 人脐带间充质干细胞源小细胞外囊泡通过抑制THBS1减轻糖尿病肾病大鼠肾脏损伤[J].江苏大学学报(医学版), 2024, 34(6):469-475.
18
Lv J, Hao YN, Wang XP, et al. Bone marrow mesenchymal stem cell-derived exosomal miR-30e-5p ameliorates high-glucose induced renal proximal tubular cell pyroptosis by inhibiting ELAVL1[J]. Ren Fail, 2023, 45(1):2177082.
19
Li M, Jiang T, Zhang W, et al. Human umbilical cord MSC-derived hepatocyte growth factor enhances autophagy in AOPP-treated HK-2 cells[J]. Exp Ther Med, 2020, 20(3):2765-2773.
20
Liu H, Wang J, Yue G, et al. Placenta-derived mesenchymal stem cells protect against diabetic kidney disease by upregulating autophagy-mediated SIRT1/FOXO1 pathway[J]. Ren Fail, 2024, 46(1):2303396.
21
Li D, Qu J, Yuan X, et al. Mesenchymal stem cells alleviate renal fibrosis and inhibit autophagy via exosome transfer of miRNA-122a[J].Stem Cells Int, 2022, 2022:1981798.
22
Liu Y, Chen J, Liang H, et al. Human umbilical cord-derived mesenchymal stem cells not only ameliorate blood glucose but also protect vascular endothelium from diabetic damage through a paracrine mechanism mediated by MAPK/ERK signaling[J]. Stem Cell Res Ther, 2022, 13(1):258.
23
Chen J, Liu Q, He J, et al.Immune responses in diabetic nephropathy: pathogenic mechanisms and therapeutic target[J]. Front Immunol, 2022, 13:958790.
24
Jo HA, Kim JY, Yang SH, et al. The role of local IL6/JAK2/STAT3 signaling in high glucose-induced podocyte hypertrophy[J]. Kidney Res Clin Pract, 2016, 35(4):212-218.
25
Hsiao PJ, Kao WY, Sung LC,et al.The role of mesenchymal stem cells in treating diabetic kidney disease:Immunomodulatory effects and kidney regeneration[J]. Int J Med Sci, 2025, 22(7):1720-1735.
26
Lin L, Lin H, Wang D, et al. Bone marrow mesenchymal stem cells ameliorated kidney fibrosis by attenuating TLR4/NF-κB in diabetic rats[J]. Life Sci, 2020, 262:118385.
27
Wang Y, Liu J, Wang H, et al. Mesenchymal stem cell-derived exosomes ameliorate diabetic kidney disease through the NLRP3 signaling pathway[J]. Stem Cells, 2023, 41(4):368-383.
28
Wang Y, Lu D, Lv S, et al. Mesenchymal stem cell-derived exosomes ameliorate diabetic kidney disease through NOD2 signaling pathway[J]. Ren Fail, 2024, 46(2):2381597.
29
Perico N, Remuzzi G, Griffin MD, et al. Nephstrom trial consortium. Safety and preliminary efficacy of mesenchymal stromal cell (ORBCEL-M) therapy in diabetic kidney disease: A randomized clinical trial (NEPHSTROM)[J]. J Am Soc Nephrol, 2023, 34(10): 1733-1751.
30
Shi Y, Wang Y, Li Q, et al. Immunoregulatory mechanisms of mesenchymal stem and stromal cells in inflammatory diseases[J]. Nat Rev Nephrol, 2018, 14(8):493-507.
31
Zhang X, Yang Y, Zhao Y. Macrophage phenotype and its relationship with renal function in human diabetic nephropathy[J]. PLoS One, 2019, 14(9):e0221991.
32
Lee SE, Jang JE, Kim HS, et al. Mesenchymal stem cells prevent the progression of diabetic nephropathy by improving mitochondrial function in tubular epithelial cells[J]. Exp Mol Med, 2019, 51(7):1-14.
33
Su W, Yin Y, Zhao J, et al. Exosomes derived from umbilical cord-derived mesenchymal stem cells exposed to diabetic microenvironment enhance M2 macrophage polarization and protect against diabetic nephropathy[J]. FASEB J, 2024, 38(14):e23798.
34
Zhu X, Wang Y, Sun Z, et al. Mesenchymal stem cells attenuate podocyte injury in diabetic nephropathy through the promotion of type 2 macrophage polarization[J]. Stem Cells Dev, 2025, 34(11-12):258-270.
35
Zhang F, Wang C, Wen X, et al. Mesenchymal stem cells alleviate rat diabetic nephropathy by suppressing CD103+ DCs-mediated CD8+ T cell responses[J]. J Cell Mol Med, 2020, 24(10):5817-5831.
36
Xue M, Zhang X, Chen J, et al. Mesenchymal stem cell-secreted TGF- β1 restores Treg/Th17 skewing induced by lipopolysaccharide and hypoxia challenge via miR-155 suppression[J]. Stem Cells Int, 2022, 2022:5522828.
37
Wang SY, Yu Y, Ge XL, et al. Causal role of immune cells in diabetic nephropathy: a bidirectional Mendelian randomization study[J]. Front Endocrinol (Lausanne), 2024, 15:1357642.
38
Liu L, Chen Y, Li X, et al.Therapeutic potential: the role of mesenchymal stem cells from diverse sources and their derived exosomes in diabetic nephropathy[J]. Biomed Pharmacother, 2024, 175:116672.
39
Rani P, Koulmane Laxminarayana SL, Swaminathan SM, et al. TGF-β: elusive target in diabetic kidney disease[J]. Ren Fail, 2025, 47(1):2483990.
40
Wu W, Wang X, Yu X, et al. Smad3 signatures in renal inflammation and fibrosis[J]. Int J Biol Sci, 2022, 18(7):2795-2806.
41
Rafiee Z, Orazizadeh M, Nejad Dehbashi F, et al. Mesenchymal stem cells derived from the kidney can ameliorate diabetic nephropathy through the TGF-β/Smad signaling pathway[J]. Environ Sci Pollut Res Int, 2022, 29(35):53212-53224.
42
Li H, Rong P, Ma X, et al. Mouse umbilical cord mesenchymal stem cell paracrine alleviates renal fibrosis in diabetic nephropathy by reducing myofibroblast transdifferentiation and cell proliferation and upregulating mmps in mesangial cells[J]. J Diabetes Res, 2020, 2020: 3847171.
43
Xu S, Cheuk YC, Jia Y, et al. Bone marrow mesenchymal stem cell-derived exosomal miR-21a-5p alleviates renal fibrosis by attenuating glycolysis by targeting PFKM[J]. Cell Death Dis, 2022, 13(10):876.
44
Zhang K, Zheng S, Wu J, et al. Human umbilical cord mesenchymal stem cell-derived Exosomes ameliorate renal fibrosis in diabetic nephropathy by targeting Hedgehog/SMO signaling[J]. FASEB J, 2024, 38(7):e23599.
45
Bian X, Conley SM, Eirin A, et al. Diabetic kidney disease induces transcriptome alterations associated with angiogenesis activity in human mesenchymal stromal cells[J]. Stem Cell Res Ther, 2023, 14(1): 49.
46
He X, Cheng R, Huang C, et al. A novel role of LRP5 in tubulointerstitial fibrosis through activating TGF-β/Smad signaling[J].Signal Transduct Target Ther, 2020, 5(1):45.
47
Hao Y, Miao J, Liu W, et al. Mesenchymal stem cell-derived exosomes carry MicroRNA-125a to protect against diabetic nephropathy by targeting histone deacetylase 1 and downregulating endothelin-1[J].Diabetes Metab Syndr Obes, 2021, 14:1405-1418.
48
Bai Y, Huang L, Fan Y, et al. Marrow mesenchymal stem cell mediates diabetic nephropathy progression via modulation of Smad2/3/WTAP/m6A/ENO1 axis [J]. FASEB J, 2024, 38(11):e23729.
49
Huang LL, Hou YY, Yang J, et al.Mitigation of ferroptosis in diabetic kidney disease through mesenchymal stem cell intervention via the Smad2/3/METTL3/S1PR1 axis[J]. FASEB J, 2025, 39(12):e70714.
50
Wu C, Mi Y, Song J, et al. The regulatory effect of human umbilical cord mesenchymal stem cells on the gut microbiota in diabetic nephropathy rats[J]. Iran J Biotechnol, 2025, 23(1):e3975.
51
Wang L, Liang A, Huang J. Exendin-4-enriched exosomes from hUCMSCs alleviate diabetic nephropathy via gut microbiota and immune modulation[J]. Front Microbiol, 2024, 15:1399632.
52
Yue Y, Yeh JN, Chiang JY, et al. Intrarenal arterial administration of human umbilical cord-derived mesenchymal stem cells effectively preserved the residual renal function of diabetic kidney disease in rat[J]. Stem Cell Res Ther, 2022, 13(1):186.
53
Takemura S, Shimizu T, Oka M, et al. Transplantation of adipose-derived mesenchymal stem cell sheets directly into the kidney suppresses the progression of renal injury in a diabetic nephropathy rat model[J]. J Diabetes Investig, 2020, 11(3):545-553.
54
Wu Z, Xu X, Cai J, et al. Prevention of chronic diabetic complications in type 1 diabetes by co-transplantation of umbilical cord mesenchymal stromal cells and autologous bone marrow: a pilot randomized controlled open-label clinical study with 8-year follow-up[J].Cytotherapy, 2022, 24(4):421-427.
55
Levy D, Jeyaram A, Born LJ, et al. Impact of storage conditions and duration on function of native and cargo-loaded mesenchymal stromal cell extracellular vesicles[J]. Cytotherapy, 2023, 25(5):502-509.
56
Chen C, Xu B, Li W, et al. New perspectives on the treatment of diabetic nephropathy: challenges and prospects of mesenchymal stem cell therapy[J]. Eur J Pharmacol, 2025, 998:177543.
[1] 何琪, 周月惠, 薛宇轩, 吉宇通, 王海彬, 周驰. 卫虚-血瘀-髓痿理论治疗激素性股骨头坏死的价值[J/OL]. 中华关节外科杂志(电子版), 2026, 20(01): 87-96.
[2] 王许杰, 李艳, 吴高峰, 官浩. 趋化因子CXC配体12预处理骨髓间充质干细胞对小鼠全层皮肤缺损创面愈合的影响及其潜在机制[J/OL]. 中华损伤与修复杂志(电子版), 2026, 21(02): 119-126.
[3] 朱君佑, 张骞, 赵止云, 甄妙, 谢举临, 李天娇, 舒斌. 色素上皮衍生因子在糖尿病创面愈合中作用机制的研究进展[J/OL]. 中华损伤与修复杂志(电子版), 2026, 21(02): 147-153.
[4] 李建雄, 杨诚, 贺慷, 薛康颐, 郭文彬, 陈明坤, 刘存东. 精索静脉曲张伴血栓形成两例报告[J/OL]. 中华腔镜泌尿外科杂志(电子版), 2026, 20(01): 114-116.
[5] 崔钰珂, 周长东, 林虹君, 李江波, 石静琦, 杨稳, 王晨辉, 董帅, 刘秀兰, 李恬, 岳洋, 郭靓. 蓝莓提取物改善特应性皮炎的作用及机制研究[J/OL]. 中华细胞与干细胞杂志(电子版), 2026, 16(02): 74-85.
[6] 邢磊, 卜玉, 张明华, 范皎. 肿瘤细胞对类泛素化抑制剂MLN4924的耐药机制及其应对措施的研究进展[J/OL]. 中华细胞与干细胞杂志(电子版), 2026, 16(02): 86-93.
[7] 方睿, 于胜强. 干细胞外泌体介导的肾脏保护:阻止纤维化进展[J/OL]. 中华细胞与干细胞杂志(电子版), 2026, 16(02): 94-101.
[8] 吴卓茜, 范圣瑾. 异基因造血干细胞移植后植入功能不良的研究进展[J/OL]. 中华细胞与干细胞杂志(电子版), 2026, 16(02): 102-109.
[9] 武文, 周振宇. 造血干细胞衰老的分子机制与干预策略[J/OL]. 中华细胞与干细胞杂志(电子版), 2026, 16(01): 39-44.
[10] 黄立政, 王玉倩, 姜金兰, 韩方雷. 间充质干细胞改善术后认知功能障碍的作用机制与研究进展[J/OL]. 中华细胞与干细胞杂志(电子版), 2026, 16(01): 45-51.
[11] 陆雅斐, 皇甫少华, 杨旭, 朱勇, 周春根, 郑正, 马传学, 王大伟, 陈澳, 林宏城, 廖联明, 江滨. 脐带间充质干细胞治疗克罗恩病肛瘘的长期疗效和安全性临床观察[J/OL]. 中华结直肠疾病电子杂志, 2026, 15(01): 72-84.
[12] 王辉, 孙咏琪. 儿童遗传性肾脏病再认识[J/OL]. 中华肾病研究电子杂志, 2026, 15(01): 8-14.
[13] 王旭, 肖昀明, 石雨申, 刘冉, 耿晓东, 王聪慧, 朱晗玉, 洪权, 张利, 陈帅印. 基于网络药理学与分子对接技术探讨济生肾气丸治疗慢性肾衰竭的机制[J/OL]. 中华肾病研究电子杂志, 2026, 15(01): 21-28.
[14] 傅志炜, 伍锦涛, 张术涛, 岳冰. 术前规律性运动可预防及缓解膝关节假体周围感染[J/OL]. 中华老年骨科与康复电子杂志, 2026, 12(01): 15-24.
[15] 高桃桃, 刘立福, 陈茵桐, 周颖璇, 邓小燕, 梁晓丽. 流行性感冒病毒继发细菌感染流行病学和致病机制研究进展[J/OL]. 中华临床实验室管理电子杂志, 2026, 14(01): 74-80.
阅读次数
全文


摘要


AI


AI小编
你好!我是《中华医学电子期刊资源库》AI小编,有什么可以帮您的吗?