Article(id=1239268421624451959, tenantId=1146029695717560320, journalId=1205117082300743687, issueId=1239268417962832543, articleNumber=null, orderNo=null, doi=10.14109/j.cnki.xyylc.2024.07.04, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1665331200000, receivedDateStr=2022-10-10, revisedDate=null, revisedDateStr=null, acceptedDate=1709222400000, acceptedDateStr=2024-03-01, onlineDate=1773394216209, onlineDateStr=2026-03-13, pubDate=1721836800000, pubDateStr=2024-07-25, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1773394216209, onlineIssueDateStr=2026-03-13, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1773394216209, creator=13701087609, updateTime=1773394216209, updator=13701087609, issue=Issue{id=1239268417962832543, tenantId=1146029695717560320, journalId=1205117082300743687, year='2024', volume='43', issue='7', pageStart='481', pageEnd='560', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1773394215336, creator=13701087609, updateTime=1773394445099, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1239269381725810851, tenantId=1146029695717560320, journalId=1205117082300743687, issueId=1239268417962832543, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1239269381725810852, tenantId=1146029695717560320, journalId=1205117082300743687, issueId=1239268417962832543, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=504, endPage=509, ext={EN=ArticleExt(id=1239268422522033022, articleId=1239268421624451959, tenantId=1146029695717560320, journalId=1205117082300743687, language=EN, title=Research progress of CD34+ cell transplantation for chronic heart failure, columnId=1207314219599499390, journalTitle=Chinese Journal of New Drugs and Clinical Remedies, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

CD34+ cells have microcirculatory regenerative potential and paracrine anti-inflammatory effects, but the number and function of CD34+ cells involved in vascular repair are decreased in patients with heart failure. Multiple trials have found that CD34+cell transplantation therapy in patients with chronic heart failure can improve myocardial performance, reduce neurohumoral activation, improve exercise capacity and quality of life, and even improve the survival rate in patients with heart failure. CD34+ cell transplantation may be a future treatment option for patients with chronic heart failure.

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CD34+细胞具有微循环再生潜能和旁分泌抗炎作用,而在心力衰竭患者中,参与血管修复的CD34+细胞数量和功能下降。多项试验发现在慢性心力衰竭患者中进行CD34+细胞移植治疗可以提高心肌性能,减少神经体液激活,并提高锻炼能力和生活质量,甚至改善心力衰竭群体的生存率。CD34+细胞移植可能成为慢性心力衰竭患者未来可选择的治疗方案。

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刘永铭,E-mail:
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王华,女,硕士在读,主要从事老年心血管病的研究,E-mail:

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王华,女,硕士在读,主要从事老年心血管病的研究,E-mail:

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CD34+细胞移植治疗慢性心力衰竭的研究进展
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王华 1 , 刘永铭 2
中国新药与临床杂志 | 综述 2024,43(7): 504-509
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中国新药与临床杂志 | 综述 2024, 43(7): 504-509
CD34+细胞移植治疗慢性心力衰竭的研究进展
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王华1 , 刘永铭2
作者信息
  • 1.兰州大学第一临床医学院,甘肃 兰州 730000
  • 2.兰州大学第一医院 老年心血管科,甘肃 兰州 730000
  • 王华,女,硕士在读,主要从事老年心血管病的研究,E-mail:

通讯作者:

刘永铭,E-mail:
Research progress of CD34+ cell transplantation for chronic heart failure
Hua WANG1 , Yong-ming LIU2
Affiliations
  • 1.The First Clinical Medical College of Lanzhou University, Lanzhou GANSU 730000, China
  • 2.Department of Geriatric Cardiology, the First Hospital of Lanzhou University, Lanzhou GANSU 730000, China
出版时间: 2024-07-25 doi: 10.14109/j.cnki.xyylc.2024.07.04
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CD34+细胞具有微循环再生潜能和旁分泌抗炎作用,而在心力衰竭患者中,参与血管修复的CD34+细胞数量和功能下降。多项试验发现在慢性心力衰竭患者中进行CD34+细胞移植治疗可以提高心肌性能,减少神经体液激活,并提高锻炼能力和生活质量,甚至改善心力衰竭群体的生存率。CD34+细胞移植可能成为慢性心力衰竭患者未来可选择的治疗方案。

抗原,CD34  /  细胞移植  /  心力衰竭

CD34+ cells have microcirculatory regenerative potential and paracrine anti-inflammatory effects, but the number and function of CD34+ cells involved in vascular repair are decreased in patients with heart failure. Multiple trials have found that CD34+cell transplantation therapy in patients with chronic heart failure can improve myocardial performance, reduce neurohumoral activation, improve exercise capacity and quality of life, and even improve the survival rate in patients with heart failure. CD34+ cell transplantation may be a future treatment option for patients with chronic heart failure.

antigens, CD34  /  cell transplantation  /  heart failure
王华, 刘永铭. CD34+细胞移植治疗慢性心力衰竭的研究进展. 中国新药与临床杂志, 2024 , 43 (7) : 504 -509 . DOI: 10.14109/j.cnki.xyylc.2024.07.04
Hua WANG, Yong-ming LIU. Research progress of CD34+ cell transplantation for chronic heart failure[J]. Chinese Journal of New Drugs and Clinical Remedies, 2024 , 43 (7) : 504 -509 . DOI: 10.14109/j.cnki.xyylc.2024.07.04
心力衰竭(心衰)是各种心脏疾病导致心功能不全的一种持续发展的综合症。左室射血分数(LVEF)可以显示心脏的功能状态,并在临床上用于对心衰进行分类。2022 AHA/ACC/HFSA指南中将慢性心衰分为4种类型,即射血分数降低的心衰(LVEF≤40%)、射血分数改善的心衰(既往LVEF≤40%,后续LVEF > 40%)、射血分数轻度降低的心衰(LVEF 41%~49%)和射血分数保留的心衰(HFpEF,LVEF≥50%)[1]。全球心衰患者超3 700万人,我国高达890万人,中重度心衰患者5年死亡率可达50%[2,3]。尽管药物治疗对缓解病情可以起到一定作用,但不能逆转心肌细胞的丧失、心室不良重塑和心功能衰退,左心室辅助设备或心脏移植等措施通常是改善晚期心衰患者预后的唯一选择。然而,可以从这些复杂且昂贵的治疗中获益的患者非常有限,且候选者的数量远远超过实际获得这些疗法的患者数量[4],因此探索有效防治措施迫在眉睫。近年来,干细胞疗法的心脏保护机制已成为研究的焦点。临床试验[5-7]数据显示,CD34+细胞在血管维持和心脏修复中起着至关重要的作用,CD34+细胞治疗不仅可以显著改善心肌细胞的灌注,还可通过干细胞衍生的旁分泌因子改善非靶向区域的灌注。最新研究发现CD34+细胞治疗的效果不仅限于左心室,还可能与右心室功能改善有关[8]。因此,CD34+细胞移植可能为心衰和右心室功能障碍患者提供益处。
CD34是一种高度糖基化的Ⅰ型跨膜糖蛋白,选择性地表达于造血干/祖细胞表面。CD34+细胞是多能造血干细胞,也称为内皮祖细胞,它包含了从早期到晚期的祖细胞,包括B细胞的祖细胞、T细胞的祖细胞以及髓系的祖细胞[9]。在过去几年里,CD34+细胞在细胞治疗临床试验和心脏疾病的生物标志物中被评估为最有说服力的细胞类型。CD34+细胞以高增殖和分化能力而闻名,在心肌损伤的修复过程中起着至关重要的作用,还可以预测心血管死亡风险[10]。同时CD34+细胞具有重要的旁分泌活性[11],可以刺激血管发生,减少内皮细胞和心肌细胞凋亡,重塑细胞外基质并激活额外的祖细胞。研究表明,整合素抗体、富含半胱氨酸蛋白61、基质细胞衍生因子1和粒细胞集落刺激因子(G-CSF)在CD34+细胞从骨髓到外周循环的动员中起着关键作用[12],当CD34+细胞转移到对应的缺血心肌组织,就会促进增强血管生成、新生血管化和组织再生,在心衰治疗中具有潜在益处[7]
CD34+细胞由于旁分泌效应及其分化成内皮细胞的能力,对衰竭的心脏修复起着十分重要的作用,MUGGERIDGE等[10]研究发现,CD34+细胞数量与全因死亡率呈负相关[危险比(HR)=0.79,95%CI:0.64~0.98,P=0.036],其中心血管疾病死亡率的HR=0.63(95%CI:0.44~0.91,P=0.013)。循环祖细胞数量的减少与血管功能障碍和随后出现的更严重的心血管风险有关,在1 281例冠状动脉(冠脉)疾病患者中发现,低CD34+细胞数量的患者在3.5年随访中,心血管死亡或心肌梗死的风险增加[13]。心血管疾病患者常表现出循环祖细胞数量的减少和血管生成能力的下降,表明患者的血管修复能力有所降低。在因心衰住院的患者中,与CD34+细胞数量高的患者相比,CD34+细胞数量低下的患者生存期缩短,表明血管修复能力受损的心衰患者死亡风险较高[14]
心衰的发展与冠脉微血管功能障碍有关,冠脉血管在影响心脏功能方面发挥着重要作用,正常心脏的微血管密度明显高于患病心脏[15]。此外,冠脉生成和心肌细胞生长之间的不平衡参与了心脏功能调节,血管受损可能导致从补偿性心脏肥大发展为失代偿心脏肥大,并最终导致心衰。因此,刺激冠脉血管生成可能是预防或逆转心衰的有利策略。研究发现,CD34+细胞能够更有效地融入缺血心肌并刺激缺血组织中的新生血管化,增加毛细血管密度,从而显著改善心肌灌注、增强心肌收缩性、降低神经体液激活、提高运动能力及总体生存率[16]。LEZAIC等[17]证实,在冠脉注射CD34+细胞6个月后,心肌灌注可显著改善。进一步研究[18]明确CD34+细胞主要通过分泌促血管生成因子,如血管内皮生长因子、白细胞介素(IL)-8、细胞因子样蛋白1等,以及分化为平滑肌细胞和血管细胞两种机制刺激内源性新生血管形成,影响病理性心脏结构和功能的重塑,并改善左心室功能[19]。此外,CD34+细胞衍生的旁分泌因子可能会进一步触发宿主心肌其他旁分泌因子的分泌,进而增强其作用。
心肌纤维化是心衰病理学的基本过程,成纤维细胞激活[20]和肌成纤维细胞产生的细胞外基质过度沉积[21]是心肌对心脏损伤的普遍反应。虽然细胞外基质合成和Ⅰ型胶原沉积的增加对愈合过程至关重要,但同时会引起心肌僵硬度增加、心肌细胞电耦合中断、氧和营养流动减少,引起左心室舒张和收缩功能障碍,并最终导致心衰[22]。心肌重构是心衰病程中最主要的解剖学特点,表现为心脏的大小、形状和收缩力随着心衰病程逐步改变。细胞外基质的稳态失调是心脏结构重塑的标志。基质金属蛋白酶(MMP)是心脏重塑的关键调节因子,通过逆向调节细胞外基质的失衡来调节心肌重构,也是心衰患者死亡和不良预后的独立预测因子。
最新研究发现,受损的心肌细胞通过激活M2巨噬细胞分泌一种β-半乳糖苷结合蛋白——半乳糖凝集素-3(galectin-3),进而通过转化生长因子(TGF)-β途径促进成纤维细胞和胶原蛋白Ⅰ在细胞外基质中增殖沉积。研究表明galectin-3与严重的心肌纤维化、心脏重塑和心衰有关[23]。POGLAJEN等[24]将心衰患者分为试验组(经心内注射CD34+细胞,n=49)与对照组(n= 18)并进行比较,发现基线galectin-3无显著差异[(13.6±5.7)ng·mL-1 vs.(13.2±4.9)ng·mL-1P=0.80]。在3个月的随访中,试验组galectin-3显著降低,而对照组有所增加[(12.1±4.0)ng·mL-1 vs.(15.7±8.4)ng·mL-1P<0.05]。该研究表明galectin-3血浆水平的降低与CD34+细胞治疗心衰的有益反应有关。CADUCEUS试验[25]显示,在冠脉内输注心肌球衍生自体干细胞12个月后,心肌的疤痕程度减轻12.3%,而对照组疤痕仅减轻了2.2%(P=0.001)。此外,干细胞组心肌收缩性改善明显大于对照组(P=0.001)。现有数据表明,干细胞治疗可能会通过抑制肿瘤坏死因子(TNF)-α和TGF-β1细胞外信号、平衡MMP和基质金属蛋白酶组织抑制因子(TIMP)的比例,以保证细胞外基质的动态稳定[26]
心衰的特点是存在持续的系统性促炎症状态[27],TNF-α、IL-6等高水平循环炎症因子会损害线粒体DNA,抑制抗氧化因子并改变线粒体复合物Ⅲ的活性,进而增加活性氧(ROS)的产生[28],ROS再通过多种机制招募循环炎症细胞和成纤维细胞祖细胞,影响多种细胞代谢途径,促进炎症介质表达,形成炎症和氧化应激的恶性循环。ROS除了加速心肌细胞死亡外,还激活并诱导许多其他类型细胞的招募,这些细胞类型不可避免地参与心肌的愈合和重塑。最值得注意的是一连串的免疫细胞,这些免疫细胞在清除坏死细胞和形成疤痕方面发挥着至关重要的作用[29]
研究发现CD34+细胞治疗的抗炎特性可能在刺激心肌的逆转重塑过程中发挥重要作用[30]。细胞治疗被证明可以通过下调促炎性细胞因子,如TNF-α、IL-1β、IL-6和单核细胞趋化蛋白1(MCP-1)的表达来抑制衰竭心肌中的促炎环境[31]。此外,干细胞可分泌具有免疫调节特性的旁分泌因子,其中最显著的是巨噬细胞集落刺激因子和TGF-β[32]
细胞治疗不仅对心肌细胞种群产生影响,而且对非心肌细胞和免疫细胞种群同样产生影响。细胞治疗除了会改变招募到损伤部位的T细胞和巨噬细胞[29],还可诱导巨噬细胞极化为修复型(M2)巨噬细胞,抑制促炎型(M1)巨噬细胞。M2巨噬细胞的特点是CD206表达增加,厌氧细胞能力增加,IL-10、TGF-β和IL-1Ra分泌增加,线粒体呼吸增加。虽然还不清楚这些变化对坏死心肌愈合过程的影响,但T细胞和巨噬细胞在清除坏死细胞和形成疤痕组织方面发挥着重要作用。HOBBY等[32]发现细胞治疗会增加巨噬细胞和CD4+T细胞,减少CD8+T细胞,并增加体内抗炎细胞因子。同时,细胞治疗会减少体内巨噬细胞的凋亡,诱导成纤维细胞的增殖,改善梗死心肌细胞的愈合环境。
非缺血性扩张性心肌病(DCM)是晚期心衰最常见的原因[33]。在55例DCM患者中,28例随机接受CD34+细胞移植(试验组),27例患者作为对照组。试验组患者通过G-CSF动员外周血中CD34+细胞,经分离收集后注射到冠脉。与基线相比,移植1年后试验组LVEF显著增加[(25.5±7.5)% vs.(30.1±6.7)%, P=0.03],6 min步行试验(6MWT)距离增加[(359±104)m vs.(485±127)m, P=0.001],N末端脑钠肽前体(NT-proBNP)下降[(2 069±1 996)pg·mL-1 vs.(1 037±950)pg·mL-1P=0.01]。此外,接受细胞治疗的患者1年死亡率或心脏移植的次要终点低于对照组(P=0.03)。随后VRTOVEC等[34]进行了更大样本量、更长时间的随访,在110例DCM患者中,55例随机接受冠脉内CD34+细胞移植,试验结果与之前一致,冠脉内干细胞移植可能与DCM患者的心室功能改善、运动耐受性和长期生存延长有关。进一步分析发现,非缺血性DCM患者冠脉内移植CD34+细胞6个月后,静息心肌灌注评分显著改善[(6.3±5.8)分vs.(3.1±4.3)分,P<0.001][17]
对缺血性心肌病患者进行心内膜CD34+细胞移植后也有相似发现[35]。一项前瞻性交叉研究纳入33例LVEF<40%的缺血性心肌病患者,第一阶段接受6个月的常规药物治疗,第二阶段所有患者接受心内膜CD34+细胞移植,随访6个月。结果发现,与第一阶段相比,患者LVEF显著改善[(27.1±6.6)% vs.(34.9±10.9)%,P=0.001],6MWT距离增加[(411±116)m vs.(496±113)m,P=0.001],NT-proBNP下降[(3 672±5 165)pg·mL-1 vs.(1 488±1 847)pg·mL-1P=0.04]。该研究同时发现,更高剂量的CD34+细胞和更分散的细胞分布与更好的临床反应有关,表明心内膜CD34+细胞移植可能与缺血性心肌病患者的左心室功能改善、NT-proBNP降低和锻炼能力提高有关。
舒张功能障碍和左心室压力升高是心衰患者生存率和症状严重性的重要预测因素。BERVAR等[36]将非缺血性DCM患者根据舒张功能将其分为两组[A组二尖瓣舒张早期血流峰值与二尖瓣环运动速度之比(E/e’)≥15;B组E/e’<15],所有患者接受心内膜CD34+细胞注射,结果表明在细胞治疗1年内,A组的E/e’在整个研究期间持续改善(-8.06,P=0.005),舒张早期与末期二尖瓣血流峰值速度比值(E/A)和舒张功能障碍等级呈下降趋势(E/A:-0.5±1.2,等级:-0.4±0.4,P=0.05), 6MWT距离显著增加[(+48±27)m,P=0.03],NT-proBNP水平下降[(-1 277±1 344)pg·mL-1P=0.02], LVEF和血压在各组间无显著差异,表明心内膜CD34+细胞移植可能会改善心脏的舒张功能,但该试验并未进行活检来排除继发性心肌病,且样本量很小,需要进一步的大型临床研究来证实是否对更广泛的心衰患者有益。
细胞治疗除了部分逆转左心室功能障碍外[37],对右心室功能的影响近年来也得到了证实。FRLJAK等[8]将60例DCM患者随机分为CD34+细胞治疗组(n=30)和对照组(n=30),治疗组接受心内膜注射CD34+细胞。在基线时,2组在年龄、性别、LVEF、NT-proBNP及右心室功能参数方面均无显著差异。6个月时,治疗组的右心室功能显著改善[三尖瓣环平面收缩期偏移(TAPSE):(+0.44±0.64)cm, P=0.001;三尖瓣环收缩期峰值运动速度(St):(+1.5±2.1)cm·s-1P=0.001;右心室面积变化分数(FAC):(+8.6 ± 5)%,P=0.01],对照组均无显著变化。治疗组有19例室间隔功能有所改善,这与右心室功能的改善有关。该研究表明,CD34+细胞疗法或许是改善慢性心衰患者右心室功能的有效干预措施。
最近一项前瞻性试验[6]共招募了30例HFpEF患者。第一阶段患者接受为期6个月的药物治疗;第二阶段患者均接受心内膜CD34+细胞移植,随访6个月。研究应用了电解剖图方法测量局部机械性舒张延迟时间和心肌活力,用以指导细胞注射的靶向性,主要终点是第一阶段和第二阶段之间E/e’变化差异。结果显示,第一阶段E/e’的变化显著小于第二阶段(-0.33±1.72 vs. -3.77±2.66,P=0.001)。第一阶段,患者整体收缩应变[GLS:(-12.5±2.4)% vs.(-12.8±2.6)%,P=0.77]、NT-proBNP [(1 463±1 247)pg·mL-1 vs.(1 298±931)pg·mL-1, P=0.31]或6MWT距离[(391±75)m vs.(402±93)m,P=0.42]无显著变化。第二阶段,NT-proBNP [(1 298±931)pg·mL-1 vs.(887±809)pg·mL-1, P=0.02]和6MWT距离[(402±93)m vs.(438±72)m, P=0.02]均有所改善。GLS在第二阶段无显著变化[(-12.8±2.6)% vs.(-13.8±2.7)%,P=0.36],但研究发现细胞注射部位的局部收缩应变有所改善[(-3.4±6.8)%,P=0.005]。这项非随机试验表明,HFpEF患者心内膜转植CD34+细胞,与细胞注射部位E/e’、NT-proBNP、运动能力和局部心肌收缩应变的改善相关。虽然该试验缺乏安慰剂对照,且HFpEF患者通常年龄较大,存在多种合并症、细胞数量减少和细胞生存能力受损等问题,自体细胞治疗对这些患者群体的影响可能有限,但试验结果可以作为进一步、更大规模试验的基础,探索细胞治疗对HFpEF患者的潜在临床益处。
大量数据表明,CD34+细胞治疗在慢性心衰患者中是可行和安全的[17,35,38]。干细胞在部分试验中失败的确切原因尚不清楚,目前普遍接受的假设是注射干细胞能够分化成成熟的心肌细胞,对缺血性心肌病患者进行的研究结果证实了这一点,其中干细胞显示再生为功能性心肌[39]。事实上,许多细胞无法分化为心肌细胞。对于干细胞疗法而言,干细胞在病变组织中的留存比例是疗效的关键。干细胞可以通过外周静脉输注、直接心肌内注射、冠脉内注射、心外膜心肌多点注射、心内膜多点注射等方式进行移植[40]。其中直接心肌内注射是多数研究推荐的移植方式之一,直接靶向目标组织,并且避免了间接方法中出现的许多复杂问题,但弊端是其植入过程的侵入性损害,且可能会引发心律失常、栓塞等突发情况。静脉输注方法简单且无创,缺点是由于细胞外逸,移植后仅有一小部分细胞最终能到达心脏,因此治疗效果不稳定。目前,非开胸手术患者推荐首选冠脉内注射,其次为静脉输注,有设备条件的可尝试行心内膜多点注射,开胸心脏手术患者根据手术方式可选择心外膜心肌多点注射、经冠脉口直接输注及冠脉搭桥术中经桥血管输注[40]
目前,CD34+细胞移植未发生严重不良事件。移植相关的轻度至中度不良事件,即骨痛和恶心,通过皮下注射重组人G-CSF均可缓解,并可根据需要服用止痛药和止吐药。有研究发现,与冠脉途径相比,心内膜CD34+细胞移植可获得更高的心肌保留率,心室功能、运动能力能获得更好的改善[41],但心肌内注射程序本身的安全性也需要仔细考虑,在注射过程中易发生心肌穿孔事件[42],随着该技术更为常规的使用,不良程序事件的发生率可能会降低。
糖尿病会对骨髓结构和功能产生负面影响,导致骨髓对动员刺激的反应减弱,循环CD34+细胞数量减少。因此,糖尿病患者的晚期心衰往往更严重,胰岛素抵抗患者需要注射更高剂量的CD34+细胞,以获得与非胰岛素抵抗患者相似的结果[43]。VRTOVEC等[44]发现非缺血性DCM患者在CD34+细胞移植后,左心室功能、运动能力和NT-proBNP水平持续改善,但长期糖尿病患者干细胞功能/心肌特性会发生改变,该类患者CD34+细胞动员能力下降。因此,糖尿病被确定为细胞治疗反应下降的重要风险因素。
综上所述,CD34+细胞疗法是一个极具前景的治疗方法,具有抗心肌纤维化、促血管生成和免疫调节等特性,可潜在刺激受损组织的修复,通过新生血管化和预防心肌细胞死亡来替换和重建受损的心肌,以改善心血管疾病患者的临床结局。但未来仍需进行大规模、多中心、随机双盲的临床研究来进一步观察CD34+细胞在心衰患者中的长期疗效。
  • 甘肃省重点研发计划(20YF8FA079)
参考文献 引证文献
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2024年第43卷第7期
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doi: 10.14109/j.cnki.xyylc.2024.07.04
  • 接收时间:2022-10-10
  • 首发时间:2026-03-13
  • 出版时间:2024-07-25
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  • 收稿日期:2022-10-10
  • 录用日期:2024-03-01
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甘肃省重点研发计划(20YF8FA079)
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    1.兰州大学第一临床医学院,甘肃 兰州 730000
    2.兰州大学第一医院 老年心血管科,甘肃 兰州 730000

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2种不同金属材料的力学参数

Family
属数
Number of
genus
种数
Number of
species
占总种数比例
Percentage of
total species (%)

Genus
种数
Number of
species
占总种数比例
Percentage of total
species (%)
鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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