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<article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" article-type="research-article" dtd-version="1.1" xml:lang="zh" xsi:noNamespaceSchemaLocation="https://jats.nlm.nih.gov/publishing/1.1/xsd/JATS-journalpublishing1.xsd"><front><journal-meta><!-- 出版商赋予期刊ID--><journal-id journal-id-type="publisher-id">YIKE</journal-id><journal-title-group><!-- 期刊中文全称--><journal-title>安徽医科大学学报</journal-title><!-- 期刊英文全称--><journal-title xml:lang="en">Acta Universitatis Medicinalis Anhui</journal-title><!-- 期刊英文缩写--><abbrev-journal-title abbrev-type="publisher" xml:lang="en">Acta Universitatis Medicinalis Anhui</abbrev-journal-title><!-- 期刊中文缩写--><abbrev-journal-title abbrev-type="publisher">安徽医科大学学报</abbrev-journal-title></journal-title-group><!-- 期刊ISSN号--><issn pub-type="ppub">1000-1492</issn><!-- 期刊CN号--><issn pub-type="cn">34-1065/R</issn><publisher><!--出版商英文名称【预置实体】 待确认 --><publisher-name xml:lang="en">Anhui Lianzhong Printing Limited Company</publisher-name><!--出版商英文地址【预置实体】 --><publisher-loc xml:lang="en">Editorial Board of Acta Universitatis Medi-cinalis Anhui Meishan Road , Hefei 230032</publisher-loc><!-- 出版商中文名称【预置实体】--><publisher-name>《安徽医科大学学报》编辑部</publisher-name><!--出版商中文地址【预置实体】 --><publisher-loc>安徽省合肥市安徽医科大学校内老图书馆三楼</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">1000–1492（2026）05–0855–06</article-id><article-id pub-id-type="doi">10.19405/j.cnki.issn1000–1492.2026.05 008</article-id><article-id pub-id-type="manuscript">V171-赵胜-血清中lncRNA-</article-id><article-categories><subj-group subj-group-type="clc"><subject>R 541</subject></subj-group><subj-group subj-group-type="dc"><subject>Ａ</subject></subj-group><subj-group subj-group-type="heading"><subject>基础医学研究</subject></subj-group></article-categories><title-group><article-title>血清中lncRNA H19和miR-22-3p对急性心肌梗死患者的诊断价值</article-title><trans-title-group xml:lang="en"><trans-title>Diagnostic value of serum lncRNA H19 and miR-22-3p in patients with acute myocardial infarction</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><name-alternatives><name name-style="eastern"><surname>赵</surname><given-names>胜</given-names></name><name name-style="eastern" xml:lang="en"><surname>Zhao</surname><given-names>Sheng</given-names></name></name-alternatives><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="author-notes" rid="fna1"/></contrib><contrib contrib-type="author"><name-alternatives><name name-style="eastern"><surname>刘</surname><given-names>定红</given-names></name><name name-style="eastern" xml:lang="en"><surname>Liu</surname><given-names>Dinghong</given-names></name></name-alternatives><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff2">2</xref><xref ref-type="aff" rid="aff3">3</xref></contrib><contrib contrib-type="author"><name-alternatives><name name-style="eastern"><surname>朱</surname><given-names>梦宇</given-names></name><name name-style="eastern" xml:lang="en"><surname>Zhu</surname><given-names>Mengyu</given-names></name></name-alternatives><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff2">2</xref><xref ref-type="aff" rid="aff3">3</xref></contrib><contrib contrib-type="author"><name-alternatives><name name-style="eastern"><surname>戎</surname><given-names>李</given-names></name><name name-style="eastern" xml:lang="en"><surname>Rong</surname><given-names>Li</given-names></name></name-alternatives><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff2">2</xref></contrib><contrib contrib-type="author"><name-alternatives><name name-style="eastern"><surname>成</surname><given-names>威</given-names></name><name name-style="eastern" xml:lang="en"><surname>Cheng</surname><given-names>Wei</given-names></name></name-alternatives><xref ref-type="aff" rid="aff1">1</xref></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern"><surname>高</surname><given-names>彦琳</given-names></name><name name-style="eastern" xml:lang="en"><surname>Gao</surname><given-names>Yanlin</given-names></name></name-alternatives><xref ref-type="aff" rid="aff1">1</xref><xref ref-type="aff" rid="aff2">2</xref><xref ref-type="corresp" rid="cor1"/><xref ref-type="author-notes" rid="fna2"/></contrib><aff-alternatives id="aff1"><aff><label>1</label><institution>安徽省第二人民医院，心内科</institution>、，<city>合肥</city>  <postal-code>230041</postal-code></aff><aff xml:lang="en"><label>1</label><institution>Department of Cardiology</institution>，</aff></aff-alternatives><aff-alternatives id="aff2"><aff><label>2</label><institution>安徽省第二人民医院，心脏中心实验室</institution>，<city>合肥</city>  <postal-code>230041</postal-code></aff><aff xml:lang="en"><label>2</label><institution>Cardiac Center Laboratory， Anhui No., Hefei</institution>　<postal-code>230041</postal-code></aff></aff-alternatives><aff-alternatives id="aff3"><aff><label>3</label><institution>蚌埠医科大学研究生院</institution>，<city>蚌埠</city>  <postal-code>233000</postal-code></aff><aff xml:lang="en"><label>3</label><institution>Provincial People's Hospital, Hefei</institution>　<postal-code>230041</postal-code></aff></aff-alternatives><aff-alternatives id="aff4"><aff xml:lang="en"><label>3</label><institution>Graduate School， Bengbu Medical University， Bengbu</institution>　<postal-code>233000</postal-code></aff></aff-alternatives></contrib-group><author-notes><corresp xml:lang="en" id="cor1"><named-content content-type="corresp-name">Gao Yanlin</named-content>， E-mail： <email>247366903@qq.com</email></corresp><fn fn-type="other" specific-use="about-author" id="fna1"><p><named-content content-type="corresp-name">赵  胜</named-content>，男，硕士， 副主任医师</p></fn><fn fn-type="other" specific-use="about-author" id="fna2"><p><named-content content-type="corresp-name">高彦琳</named-content>，女，硕士， 副主任医师，通信作者，E-mail： 24736 <email>6903@qq.com</email></p></fn></author-notes><pub-date pub-type="epub" iso-8601-date="2026-04-26T10：43：45"><day>26</day><month>04</month><year>2026</year></pub-date>    <history><date date-type="received">       <day>26</day><month>02</month><year>2026</year></date>  </history><pub-date pub-type="ppub"><day>23</day><month>05</month><year>2026</year></pub-date><volume>61</volume><issue>5</issue><issue-id>16</issue-id><fpage>855</fpage><lpage>860</lpage><page-range>855-860</page-range><abstract abstract-type="key-points"><sec><title>目的</title><p>探究长链非编码RNA（lncRNA）H19和微小RNA-22-3p（miR-22-3p）在急性心肌梗死（AMI）患者血清中的表达水平及其对AMI诊断的价值。</p></sec><sec><title>方法</title><p>选取176例AMI患者为试验组，根据患者病史资料和心电图分为ST段抬高型心肌梗死（STEMI）组（<italic>n</italic>=95）和非ST段抬高型心肌梗死（NSTEMI）组（<italic>n</italic>=81）以及同期入院的156例造影阴性者为对照（CON）组，采用实时荧光定量聚合酶链反应方法检测2组血清中lncRNA H19和miR-22-3p相对表达量的差异，应用受试者操作特征（ROC）曲线分析血清中miR-22-3p和lncRNA H19在AMI中的诊断价值。检测所有研究对象血清肌钙蛋白I（cTnI）和肌酸激酶（CK）、肌酸激酶MB同工酶（CK-MB）、超敏C反应蛋白（CRP）的水平。采用Spearman相关性分析评估lncRNA H19和miR-22-3p与cTnI、CK、CK-MB及CRP的相关性。</p></sec><sec><title>结果</title><p>与CON组相比，AMI组lncRNA H19表达水平上调，miR-22-3p表达水平下调（均<italic>P</italic>&lt;0.01）；与NSTEMI组相比，STEMI组 lncRNA H19表达水平上调，miR-22-3p表达水平下调（<italic>P</italic>&lt;0.01）；miR-22-3p、lncRNA H19和两者联合对AMI诊断预测的ROC曲线下面积（AUC）分别为 0.555、0.977、0.983；lncRNA H19与cTnI、CK、CK-MB、CRP呈正相关（<italic>P</italic>&lt;0.05），与左室射血分数（LVEF）呈负相关（<italic>P</italic>&lt;0.001）；miR-22-3p与cTnI、CK、CRP呈负相关，与LVEF呈正相关（<italic>P</italic>&lt;0.05）。</p></sec><sec><title>结论</title><p>AMI患者中血清lncRNA H19 表达水平升高，miR-22-3p表达水平降低，并且其水平对AMI患者具有一定的辅助诊断及心功能评估意义。</p></sec></abstract><trans-abstract abstract-type="key-points" xml:lang="en"><sec><title>Objective</title><p>To explore the expression levels of long non-coding RNA （lncRNA） H19 and microRNA-22-3p （miR-22-3p） in the serum of patients with acute myocardial infarction （AMI） and their diagnostic value for AMI.</p></sec><sec><title>Methods</title><p>A total of 176 AMI patients were selected as the experimental group and were divided into ST-segment elevation myocardial infarction （STEMI） group （<italic>n</italic>=95） and non-ST-segment elevation myocardial infarction （NSTEMI） group （<italic>n</italic>=81） based on their medical history and electrocardiogram. Meanwhile， 156 patients with negative angiography during the same period were selected as the control group （CON group）. The relative expression levels of lncRNA H19 and miR-22-3p in the serum of the two groups were detected by real-time fluorescence quantitative polymerase chain reaction. The diagnostic value of miR-22-3p and lncRNA H19 in AMI was evaluated by receiver operating characteristic curve （ROC） analysis. The levels of serum cardiac troponin I （cTnI）， creatine kinase （CK）， creatine kinase MB isoenzyme （CK-MB）， and high-sensitivity C-reactive protein （CRP） were detected in all study subjects. Spearman correlation analyses were used to evaluate the correlations between lncRNA H19 and miR-22-3p and cTnI， CK， CK-MB and CRP.</p></sec><sec><title>Results</title><p>Compared with the control group， the expression level of lncRNA H19 was upregulated and the expression level of miR-22-3p was downregulated in the AMI group （all <italic>P</italic>&lt;0.01）； compared with the NSTEMI group， the expression level of lncRNA H19 was upregulated and the expression level of miR-22-3p was downregulated in the STEMI group （<italic>P</italic>&lt;0.01）. The areas under the ROC curves （AUC） for the diagnosis of AMI by miR-22-3p， lncRNA H19 and their combination were 0.555， 0.977， and 0.983， respectively. lncRNA H19 was positively correlated with cTnI， CK， CK-MB and CRP （<italic>P</italic>&lt;0.05）， and negatively correlated with left ventricular ejection fraction （LVEF） （<italic>P</italic>&lt;0.001）； miR-22-3p was negatively correlated with cTnI， CK and CRP， and positively correlated with LVEF （<italic>P</italic>&lt;0.05）.</p></sec><sec><title>Conclusion</title><p>The expression level of lncRNA H19 is elevated and the expression level of miR-22-3p decreased in AMI patients， and their levels may have potential value as an auxiliary biomarker for AMI diagnosis and cardiac function assessment.</p></sec></trans-abstract><kwd-group kwd-group-type="author"><kwd>长链非编码RNA</kwd><kwd>lncRNA H19</kwd><kwd>miR-22-3p</kwd><kwd>急性心肌梗死</kwd><kwd>心功能</kwd></kwd-group><kwd-group xml:lang="en" kwd-group-type="author"><kwd>long non-coding RNA</kwd><kwd>lncRNA H19</kwd><kwd>miR-22-3p</kwd><kwd>acute myocardial infarction</kwd><kwd>cardiac function</kwd></kwd-group><funding-group><award-group><funding-source>安徽省卫生健康科研项目</funding-source><award-id>AHWJ2024Bai30022</award-id></award-group><award-group><funding-source>安徽省高校自然科学研究项目</funding-source><award-id>2023AH053377</award-id></award-group><funding-statement>安徽省卫生健康科研项目（编号：AHWJ2024Bai30022）；安徽省高校自然科学研究项目（编号：2023AH053377）</funding-statement></funding-group><funding-group xml:lang="en"><award-group><funding-source>Health Research Project of Anhui Province</funding-source><award-id>AHWJ2024Bai30022</award-id></award-group><award-group><funding-source>Natural Science Research Project of Anhui Educational Committee</funding-source><award-id>2023AH053377</award-id></award-group><funding-statement>Health Research Project of Anhui Province （No. AHWJ2024Bai30022）； Natural Science Research Project of Anhui Educational Committee （No. 2023AH053377）</funding-statement></funding-group><counts><fig-count count="3"/><table-count count="3"/><equation-count count="0"/><ref-count count="19"/><page-count count="6"/><word-count count="16007"/></counts><custom-meta-group><custom-meta><meta-name>version</meta-name><meta-value>1.0.0.25091</meta-value></custom-meta><custom-meta><meta-name>structure-time</meta-name><meta-value>2026-06-30T11:07:19</meta-value></custom-meta><custom-meta><meta-name>word-source</meta-name><meta-value>FX</meta-value></custom-meta></custom-meta-group></article-meta></front><body><p>急性心肌梗死（acute myocardial infarction， AMI）为冠状动脉斑块破裂导致血栓形成而引起心肌组织持续缺血坏死，具有较高的致死致残率<sup>［<xref ref-type="bibr" rid="R1">1</xref>］</sup>。目前心电图、心肌酶等是其确诊的主要手段，但寻找更新的评估指标仍是目前临床研究重点。近年来，研究<sup>［<xref ref-type="bibr" rid="R2">2</xref>–<xref ref-type="bibr" rid="R3">3</xref>］</sup>表明非编码RNA能通过参与基因和蛋白质调控在多种疾病进展方面发挥作用。长链非编码RNA（lncRNA）作为非编码RNA之一，能通过基因调控和细胞信号传导路径影响心血管细胞功能和行为，在心肌细胞的增殖分化以及血管新生和血管平滑肌细胞功能调控中发挥作用<sup> ［<xref ref-type="bibr" rid="R2">2</xref>，<xref ref-type="bibr" rid="R4">4</xref>–<xref ref-type="bibr" rid="R5">5</xref>］</sup>，但在AMI中的表达情况尚不明确。微小RNA-22-3p（miR-22-3p）是心脏中表达最丰富的非编码RNA之一，并受到lncRNA H19调控<sup>［<xref ref-type="bibr" rid="R6">6</xref>］</sup>。既往研究<sup>［<xref ref-type="bibr" rid="R7">7</xref>］</sup>表明循环血单核细胞中的miR-22-3p在冠心病患者中表达升高，但其在AMI中的变化情况及潜在机制未被充分研究。该研究比较分析了AMI患者与冠脉造影排除冠心病的对照组患者的血清样本，旨在评估lncRNA H19和miR-22-3p在AMI诊断中的潜在作用，并探讨其在临床诊断与治疗方面的应用价值。</p><sec id="s1"><label>1</label><title>材料与方法</title><sec id="s1a"><label>1.1</label><title>病例资料</title><p specific-use="noneIndent">根据AMI诊疗指南<sup>［<xref ref-type="bibr" rid="R8">8</xref>］</sup>选取2021年1月—2024年12月安徽省第二人民医院心血管内科AMI患者176例为疾病组，后根据心电图检查结果分为ST段抬高型心肌梗死组（STEMI组，95例）和非ST段抬高型心肌梗死组（NSTEMI组，81例），选取同期经冠脉造影提示非冠心病的患者156例为对照组（CON组）。AMI纳入标准：① 符合AMI诊断标准；② 年龄≥29岁；③ 入院时仍有心肌梗死症状。排除标准：① 既往心脏病手术病史；② 合并其他重大疾病，如恶性肿瘤、血液系统疾病等；③ 药物不耐受或过敏患者；④ 怀孕或哺乳期患者；⑤ 参与其他临床试验研究；⑥ 合并精神疾病；⑦ 临床资料不完整。本研究经安徽省第二人民医院医学伦理委员会批准（批号：2022-008），所有研究对象均签署知情同意书。</p></sec><sec id="s1b"><label>1.2</label><title>临床资料收集</title><p specific-use="noneIndent">对于所有研究对象，详细记录关键的个人信息和健康背景，包括每位参与者的年龄、性别、吸烟饮酒史、高血压和糖尿病的发病情况等。</p></sec><sec id="s1c"><label>1.3</label><title>实时荧光定量聚合酶链反应（quantitative real-time PCR， qPCR）检测lncRNA H19和miR-22-3p在血清中的含量</title><sec id="s1c1"><label>1.3.1</label><title>主要仪器和试剂</title><p specific-use="noneIndent">定量PCR仪（型号ABI700）购自美国Applied Biosystems公司；高速冷冻离心机（型号A22K-ER）购自湖南安君研仪器有限公司；紫外分光光度仪器（型号3900H）购自日本日立公司。改良型TRIzol试剂购自美国BioTools公司；microRNA转录合成套件购自中国GenScript生物科技公司；Long-Chain RNA转录套件、Long RNA Quantitative PCR试剂盒购自中国BioWise生物科技公司； Green miRNA RT-PCR试剂盒购自美国GeneCopoeia公司。</p></sec><sec id="s1c2"><label>1.3.2</label><title>实验方法</title><p specific-use="noneIndent">在AMI和CON组入院后24 h内从静脉抽取5 mL血液，使用3 500 r/min离心10 min以分离血清。改良型TRIzol试剂提取血清中总RNA，通过琼脂糖凝胶电泳或分光光度计测定RNA的浓度和纯度。从合格的RNA样品中取适量RNA，使用microRNA转录合成套件和Long-Chain RNA转录套件进行cDNA合成。利用Green miRNA RT-PCR试剂盒和Long RNA Quantitative PCR试剂盒进行PCR扩增，qPCR系统测定lncRNA H19和miR-22-3p的相对表达量。实验结束后，以3-磷酸甘油醛脱氢酶（<italic>GAPDH</italic>）和<italic>U6</italic>为内参基因，采用2<sup>-ΔΔ</sup><italic><sup>C</sup></italic><inline-formula><alternatives><mml:math id="M1"><mml:msub><mml:mrow/><mml:mrow><mml:mi mathvariant="normal">T</mml:mi></mml:mrow></mml:msub></mml:math><graphic specific-use="big" xlink:href="alternativeImage/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-M001.jpg"><?fx-imagestate width="1.26999998" height="4.23333359"?></graphic><graphic specific-use="small" xlink:href="alternativeImage/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-M001c.jpg"><?fx-imagestate width="1.26999998" height="4.23333359"?></graphic></alternatives></inline-formula>方法进行表达量的相对定量分析，见<xref ref-type="table" rid="T1">表1</xref>。</p><table-wrap id="T1"><object-id pub-id-type="doi">10.19405/j.cnki.issn1000–1492.2026.05.008.T001</object-id><label>表1</label><caption><p>RT-PCR引物序列</p></caption><abstract abstract-type="caption" xml:lang="en"><label>Tab.1</label><title>RT-PCR primer sequences</title></abstract><alternatives><table id="Table1"><thead><tr><th align="left" style="border-top:solid;border-bottom:solid;">Primer name</th><th align="center" colspan="2" style="border-top:solid;border-bottom:solid;">Primer sequence（5′-3′）</th></tr></thead><tbody><tr align="center"><td align="left" rowspan="2">miR-22-3p</td><td align="left"/><td align="left">F：TGCTGCCAGTTGAAGAACTGT</td></tr><tr align="center"><td align="left"/><td align="left">R：CTCAACTGGTGTCGTGGAGTC</td></tr><tr align="center"><td align="left" rowspan="2">lncRNA H19</td><td align="left"/><td align="left">F：TAAAGCAGCTGGGGTGGTGAG</td></tr><tr align="center"><td align="left"/><td align="left">R：TGACTGGCAGGCACATCCAC</td></tr><tr align="center"><td align="left" rowspan="2">GAPDH</td><td align="left"/><td align="left">F：ACAGCAACAGGGTGGTGGAC</td></tr><tr align="center"><td align="left"/><td align="left">R：TTTGAGGGTGCAGCGAACTT</td></tr><tr align="center"><td align="left" rowspan="2" style="border-bottom:solid;">U6</td><td align="left"/><td align="left">F：CCTGCTTCGGCAGCACAT</td></tr><tr align="center"><td align="left" style="border-bottom:solid;"/><td align="left" style="border-bottom:solid;">R：AACGCTTCACGAATTTGCGT</td></tr></tbody></table><graphic specific-use="big" xlink:href="alternativeImage/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-T001.jpg"><?fx-imagestate width="81.19583893" height="41.34600830"?></graphic><graphic specific-use="small" xlink:href="alternativeImage/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-T001c.jpg"><?fx-imagestate width="81.19583893" height="41.34600830"?></graphic></alternatives></table-wrap></sec></sec><sec id="s1d"><label>1.4</label><title>心功能指标测定</title><p specific-use="noneIndent">使用彩色多普勒心脏诊断仪（型号：EPIQ 7C，荷兰Philips公司）对参与者进行心脏超声检查，测量包括左心房内径（left atrial diameter， LAD）及左室射血分数（left ventricular ejection fraction， LVEF）等指标。利用酶联免疫吸附试验（enzyme linked immunosorbent assay，ELISA）测定受试者血清中的关键生化指标。检测指标包括血清肌钙蛋白I（cardiac troponin I， cTnI）、肌酸激酶（creatine kinase， CK）、肌酸激酶MB同工酶（creatine kinase-MB ， CK-MB）、乳酸脱氢酶（lactate dehydrogenase， LDH）及C反应蛋白（C-reactive protein， CRP）。上述检测所需的试剂盒均采购自武汉依莱瑞特生物有限公司。</p></sec><sec id="s1e"><label>1.5</label><title>统计学处理</title><p specific-use="noneIndent">使用SPSS 23.0和Origin 9.1进行数据分析。首先对数据进行正态性检验。对于服从正态分布的数据，使用<inline-formula><alternatives><mml:math id="M2"><mml:mover accent="true"><mml:mi>x</mml:mi><mml:mo>¯</mml:mo></mml:mover><mml:mo>±</mml:mo><mml:mi>s</mml:mi></mml:math><graphic specific-use="big" xlink:href="alternativeImage/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-M002.jpg"><?fx-imagestate width="7.53533268" height="2.70933342"?></graphic><graphic specific-use="small" xlink:href="alternativeImage/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-M002c.jpg"><?fx-imagestate width="7.53533268" height="2.70933342"?></graphic></alternatives></inline-formula>来描述，并通过独立样本的<italic>t</italic>检验来比较不同组之间的差异。对于不服从正态分布的数据，则采用<italic>M</italic>（<italic>P</italic><sub>25</sub>， <italic>P</italic><sub>75</sub>）表示，并使用Mann-Whitney <italic>U</italic>检验进行组间比较。计数数据以<italic>n</italic>（%）的形式呈现。不同组别间的计数数据比较通过<italic>χ</italic><sup>2</sup>检验来执行。对lncRNA H19和miR-22-3p与心功能指标间的相关性进行分析，根据数据的特性采用Spearman双变量相关性分析。利用受试者操作特征（receiver operating characteristic， ROC）曲线评估lncRNA H19和miR-22-3p对于AMI诊断的预测价值。以<italic>P</italic>&lt;0.05为差异有统计学意义。</p></sec></sec><sec id="s2"><label>2</label><title>结果</title><sec id="s2a"><label>2.1</label><title>AMI组与CON组基本资料比较</title><p specific-use="noneIndent">AMI组与CON组在年龄、饮酒史及糖尿病史等临床资料方面差异无统计学意义；AMI组男性比例及高血压比例高于CON组（<italic>P</italic>&lt;0.05）。AMI组CRP、cTnI、CK、CK-MB和LDH高于CON组，而LVEF低于CON组，差异有统计学意义（<italic>P</italic>&lt;0.001）。见<xref ref-type="table" rid="T2">表2</xref>。</p><table-wrap id="T2"><object-id pub-id-type="doi">10.19405/j.cnki.issn1000–1492.2026.05.008.T002</object-id><label>表2</label><caption><p>两组临床资料比较 ［<inline-formula><alternatives><mml:math id="M3"><mml:mover accent="true"><mml:mi>x</mml:mi><mml:mo>¯</mml:mo></mml:mover></mml:math><graphic specific-use="big" xlink:href="alternativeImage/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-M003.jpg"><?fx-imagestate width="1.35466671" height="2.03200006"?></graphic><graphic specific-use="small" xlink:href="alternativeImage/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-M003c.jpg"><?fx-imagestate width="1.35466671" height="2.03200006"?></graphic></alternatives></inline-formula><italic>±s， n</italic>（<italic>%</italic>）<italic>， M</italic>（<italic>P</italic><sub>25</sub><italic>， P</italic><sub>75</sub>）］</p></caption><abstract abstract-type="caption" xml:lang="en"><label>Tab.2</label><title>Comparison of clinical data between the two groups ［<inline-formula><alternatives><mml:math id="M4"><mml:mover accent="true"><mml:mi>x</mml:mi><mml:mo>¯</mml:mo></mml:mover></mml:math><graphic specific-use="big" xlink:href="alternativeImage/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-M003.jpg"><?fx-imagestate width="1.35466671" height="2.03200006"?></graphic><graphic specific-use="small" xlink:href="alternativeImage/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-M003c.jpg"><?fx-imagestate width="1.35466671" height="2.03200006"?></graphic></alternatives></inline-formula><italic>±s， n</italic>（<italic>%</italic>）<italic>， M</italic>（<italic>P</italic><sub>25</sub><italic>， P</italic><sub>75</sub>）］</title></abstract><alternatives><table id="Table2"><thead><tr><th align="left" style="border-top:solid;border-bottom:solid;">Clinical data</th><th align="center" style="border-top:solid;border-bottom:solid;">CON group （<italic>n</italic>=156）</th><th align="center" style="border-top:solid;border-bottom:solid;">AMI group（<italic>n</italic>=176）</th><th align="center" style="border-top:solid;border-bottom:solid;"><italic>P </italic>value</th></tr></thead><tbody><tr align="center"><td align="justify">Age （years）</td><td align="center">59.49±12.64</td><td align="center">59.81±13.62</td><td align="center">0.826</td></tr><tr align="center"><td align="justify">Male</td><td align="center">98（62.82）</td><td align="center">136（77.27）</td><td align="center">0.004</td></tr><tr align="center"><td align="left">Alcohol drinking</td><td align="center">43（27.56）</td><td align="center">61（34.66）</td><td align="center">0.164</td></tr><tr align="center"><td align="left">Diabetes</td><td align="center">24（15.38）</td><td align="center">26（14.77）</td><td align="center">0.876</td></tr><tr align="center"><td align="left">Hypertension</td><td align="center">73（48.72）</td><td align="center">105（59.66）</td><td align="center">0.019</td></tr><tr align="center"><td align="left">LAD （mm）</td><td align="center">34.41±5.11</td><td align="center">35.35±4.50</td><td align="center">0.079</td></tr><tr align="center"><td align="left">LVEF （%）</td><td align="center">65.00 （62.00， 67.00）</td><td align="center">61.00 （53.00， 65.00）</td><td align="center">&lt;0.001</td></tr><tr align="center"><td align="left">CRP （mg/L）</td><td align="center">5.00（1.70， 6.20）</td><td align="center">5.60（4.48， 13.41）</td><td align="center">&lt;0.001</td></tr><tr align="center"><td align="left">cTnI （ng/L）</td><td align="center">0.01（0.01， 0.01）</td><td align="center">0.58（0.08， 3.46）</td><td align="center">&lt;0.001</td></tr><tr align="center"><td align="left">CK （U/L）</td><td align="center">68.00（50.00， 104.00）</td><td align="center">146.00（81.50， 358.50）</td><td align="center">&lt;0.001</td></tr><tr align="center"><td align="left">CK-MB （U/L）</td><td align="center">9.00（5.00， 12.00）</td><td align="center">19.00（11.0， 48.00）</td><td align="center">&lt;0.001</td></tr><tr align="center"><td align="left" style="border-bottom:solid;">LDH （U/L）</td><td align="center" style="border-bottom:solid;">171.00（150.00， 205.00）</td><td align="center" style="border-bottom:solid;">233.00（167.50， 361.00）</td><td align="center" style="border-bottom:solid;">&lt;0.001</td></tr></tbody></table><graphic specific-use="big" xlink:href="alternativeImage/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-T002.jpg"><?fx-imagestate width="169.79998779" height="59.72200012"?></graphic><graphic specific-use="small" xlink:href="alternativeImage/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-T002c.jpg"><?fx-imagestate width="169.79998779" height="59.72200012"?></graphic></alternatives></table-wrap></sec><sec id="s2b"><label>2.2</label><title>AMI组和CON组lncRNA H19和miR-22-3p的表达</title><p specific-use="noneIndent">qPCR检测结果显示，与CON组相比，AMI组lncRNA H19水平升高，miR-22-3p水平降低（<italic>P</italic>&lt;0.01）；AMI患者亚组分析显示，STEMI组lncRNA H19高于NSTEMI组而miR-22-3p水平低于NSTEMI组（均<italic>P</italic>&lt;0.01）。见图<xref ref-type="fig" rid="F1">1</xref>、<xref ref-type="fig" rid="F2">2</xref>。</p><fig position="float" id="F1"><object-id pub-id-type="doi">10.19405/j.cnki.issn1000–1492.2026.05.008.F001</object-id><label>图1</label><caption><title>qPCR测定不同分组中lncRNA H19的相对表达量</title></caption><abstract abstract-type="caption" xml:lang="en"><label>Fig.1</label><title>qPCR determination of the relative expression of lncRNA H19 in different groups</title></abstract><abstract abstract-type="note"><p><sup>**</sup><italic>P</italic>&lt;0.01 <italic>vs</italic> CON group； <sup>##</sup><italic>P</italic>&lt;0.01 <italic>vs</italic> NSTEMI group.</p></abstract><alternatives><graphic specific-use="print" xlink:href="media/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-F001.eps" id="Graphic1"><?fx-imagestate width="72.67222595" height="59.61944962"?></graphic><graphic specific-use="big" xlink:href="alternativeImage/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-F001.jpg"><?fx-imagestate width="72.67222595" height="59.61944962"?></graphic><graphic specific-use="small" xlink:href="alternativeImage/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-F001c.jpg"><?fx-imagestate width="72.67222595" height="59.61944962"?></graphic></alternatives></fig><fig position="float" id="F2"><object-id pub-id-type="doi">10.19405/j.cnki.issn1000–1492.2026.05.008.F002</object-id><label>图2</label><caption><title>qPCR测定不同分组中miR-22-3p的相对表达量</title></caption><abstract abstract-type="caption" xml:lang="en"><label>Fig.2</label><title>qPCR determination of the relative expression of miR-22-3p in different groups</title></abstract><abstract abstract-type="note"><p><sup>**</sup><italic>P</italic>&lt;0.01 <italic>vs</italic> CON group； <sup>##</sup><italic>P</italic>&lt;0.01 <italic>vs</italic> NSTEMI group.</p></abstract><alternatives><graphic specific-use="print" xlink:href="media/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-F002.eps" id="Graphic2"><?fx-imagestate width="72.67222595" height="59.97222519"?></graphic><graphic specific-use="big" xlink:href="alternativeImage/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-F002.jpg"><?fx-imagestate width="72.67222595" height="59.97222519"?></graphic><graphic specific-use="small" xlink:href="alternativeImage/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-F002c.jpg"><?fx-imagestate width="72.67222595" height="59.97222519"?></graphic></alternatives></fig></sec><sec id="s2c"><label>2.3</label><title>ROC曲线评估lncRNA H19和miR-22-3p对AMI组的诊断价值</title><p specific-use="noneIndent">在ROC曲线分析中，miR-22-3p对AMI的诊断效能AUC为0.555（95% <italic>CI</italic>：0.493~0.617），其敏感度和特异性分别为59.6%和52.8%，miR-22-3p单独诊断效能有限。lncRNA H19的诊断AUC为0.977（95% <italic>CI</italic>：0.963~0.990），对应的敏感度和特异性分别为91.5%和94.9%。两者联合诊断后AUC值为0.983（95% <italic>CI</italic>：0.972~0.994），此时敏感度为93.8%，特异性为94.9%。见<xref ref-type="fig" rid="F3">图3</xref>。</p><fig position="float" id="F3"><object-id pub-id-type="doi">10.19405/j.cnki.issn1000–1492.2026.05.008.F003</object-id><label>图3</label><caption><title>miR-22-3p、lncRNA H19及lncRNA H19与miR-22-3p联合对AMI诊断的ROC曲线</title></caption><abstract abstract-type="caption" xml:lang="en"><label>Fig.3</label><title>ROC curve of AMI diagnosis by miR-22-3p， lncRNA H19，and the combination of lncRNA H19 and miR-22-3p</title></abstract><alternatives><graphic specific-use="print" xlink:href="media/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-F003.eps" id="Graphic3"><?fx-imagestate width="73.37777710" height="63.85277557"?></graphic><graphic specific-use="big" xlink:href="alternativeImage/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-F003.jpg"><?fx-imagestate width="73.37777710" height="63.85277557"?></graphic><graphic specific-use="small" xlink:href="alternativeImage/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-F003c.jpg"><?fx-imagestate width="73.37777710" height="63.85277557"?></graphic></alternatives></fig></sec><sec id="s2d"><label>2.4</label><title>血清中lncRNA H19和miR-22-3p与心肌损伤指标的相关性</title><p specific-use="noneIndent">Spearman分析AMI组血清lncRNA H19和miR-22-3p与心肌损伤指标的相关性结果显示，lncRNA H19与cTnI、CK、CK-MB、CRP呈正相关（<italic>P</italic>&lt;0.05），与LVEF呈负相关（<italic>P</italic>&lt;0.001）；miR-22-3p与cTnI、CK、CRP呈负相关，与LVEF呈正相关（<italic>P</italic>&lt;0.05），但miR-22-3p与CK-MB相关性差异无统计学意义。见<xref ref-type="table" rid="T3">表3</xref>。</p><table-wrap id="T3"><object-id pub-id-type="doi">10.19405/j.cnki.issn1000–1492.2026.05.008.T003</object-id><label>表3</label><caption><p>lncRNA H19和miR-22-3p与心肌损伤指标的相关性</p></caption><abstract abstract-type="caption" xml:lang="en"><label>Tab.3</label><title>Correlation between lncRNA H19 and miR-22-3p and indicators of myocardial injury</title></abstract><alternatives><table id="Table3"><thead><tr><th align="left" rowspan="2" style="border-top:solid;border-bottom:solid;">Clinical indicator</th><th align="center" colspan="2" style="border-top:solid;border-bottom:solid;">lncRNA H19</th><th align="center" colspan="2" style="border-top:solid;border-bottom:solid;">miR-22-3p</th></tr><tr><th align="center" style="border-bottom:solid;"><italic>r </italic>value</th><th align="center" style="border-bottom:solid;"><italic>P </italic>value</th><th align="center" style="border-bottom:solid;"><italic>r </italic>value</th><th align="center" style="border-bottom:solid;"><italic>P </italic>value</th></tr></thead><tbody><tr align="center"><td align="left">cTnI</td><td align="center">0.666</td><td align="center">&lt;0.001</td><td align="center">-0.115</td><td align="center">0.038</td></tr><tr align="center"><td align="left">CK</td><td align="center">0.399</td><td align="center">&lt;0.001</td><td align="center">-0.158</td><td align="center">0.004</td></tr><tr align="center"><td align="left">CK-MB</td><td align="center">0.453</td><td align="center">&lt;0.001</td><td align="center">-0.111</td><td align="center">0.331</td></tr><tr align="center"><td align="left">CRP</td><td align="center">0.234</td><td align="center">0.025</td><td align="center">-0.106</td><td align="center">0.045</td></tr><tr align="center"><td align="left" style="border-bottom:solid;">LVEF</td><td align="center" style="border-bottom:solid;">-0.385</td><td align="center" style="border-bottom:solid;">&lt;0.001</td><td align="center" style="border-bottom:solid;">0.119</td><td align="center" style="border-bottom:solid;">0.030</td></tr></tbody></table><graphic specific-use="big" xlink:href="alternativeImage/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-T003.jpg"><?fx-imagestate width="81.19583130" height="34.29999924"?></graphic><graphic specific-use="small" xlink:href="alternativeImage/45C805F0-1A67-4e98-B2E2-CB59EFFC558B-T003c.jpg"><?fx-imagestate width="81.19583130" height="34.29999924"?></graphic></alternatives></table-wrap></sec></sec><sec id="s3"><label>3</label><title>讨论</title><p>AMI是由冠状动脉急性闭塞导致心肌持续缺血坏死所致的严重心血管事件<sup>［<xref ref-type="bibr" rid="R1">1</xref>］</sup>。目前临床初次诊断主要依赖心电图及心肌损伤标志物，尤其是肌钙蛋白。然而，在慢性肾功能不全、心力衰竭及炎症状态下，肌钙蛋白亦可能升高，提示其特异性在某些临床情境下受到影响。从不同病理信息维度反映心肌损伤的新型分子标志物探究已成为当前研究热点。</p><p>近年来，非编码RNA在心血管疾病中的作用受到了广泛关注，尤其是lncRNA<sup>［<xref ref-type="bibr" rid="R9">9</xref>］</sup>。lncRNA是一类长度超过200个核苷酸的RNA分子，它们不编码蛋白质，但在调节基因表达方面发挥着重要作用，包括与蛋白质、DNA及其他RNA的互作，影响基因的激活或抑制<sup>［<xref ref-type="bibr" rid="R10">10</xref>］</sup>。lncRNA H19位于人类11号染色体<italic>H19</italic>基因的端粒区附近，能通过基因表达调控、表观遗传修饰和细胞信号传导路径影响心血管细胞的功能和行为并可能在缺血再灌注损伤中发挥作用<sup>［<xref ref-type="bibr" rid="R4">4</xref>–<xref ref-type="bibr" rid="R5">5</xref>］</sup>。既往研究<sup>［<xref ref-type="bibr" rid="R5">5</xref>， <xref ref-type="bibr" rid="R11">11</xref>–<xref ref-type="bibr" rid="R12">12</xref>］</sup>显示lncRNA H19和miR-22-3p在心血管系统的稳态维护中扮演重要角色。Omura et al<sup>［<xref ref-type="bibr" rid="R13">13</xref>］</sup>研究发现lncRNA H19是肺动脉高压右心室功能衰竭的潜在标志物和治疗靶点。李锦爽 等<sup>［<xref ref-type="bibr" rid="R14">14</xref>］</sup>发现AMI早期患者血清lncRNA H19明显升高，并且升高的lncRNA H19对AMI患者远期心脏重构具有预测价值。但有研究<sup>［<xref ref-type="bibr" rid="R15">15</xref>］</sup>显示，升高的lncRNA H19可能通过发挥miR-139、miR-22的内源性海绵作用减少下游靶分子的降解，从而对缺血缺氧的心肌发挥保护作用。因此，lncRNA H19在心血管疾病中具有双向调节作用。本研究在人群层面发现AMI患者血清lncRNA H19表达水平升高，且与cTnI、CK及CK-MB等心肌损伤指标呈正相关，提示其表达水平可能与心肌细胞损伤程度相关。既往有研究<sup>［<xref ref-type="bibr" rid="R16">16</xref>–<xref ref-type="bibr" rid="R17">17</xref>］</sup>提示lncRNA H19可能参与炎症调控过程，本研究结果显示，AMI患者血清lncRNA H19水平与CRP呈弱正相关（<italic>r</italic>=0.234，<italic>P</italic>=0.025），但其与cTnI、CK、CK-MB等心肌损伤标志物的相关系数（<italic>r</italic>=0.666、0.399、0.453）均明显高于与CRP的相关性，提示在AMI急性期，lncRNA H19的表达变化可能更多地反映心肌细胞结构损伤的程度，而非单纯的机体炎症反应水平。lncRNA H19在不同病理状态下可能发挥双向调节作用，其在AMI急性期中的具体功能仍需进一步机制研究阐明。</p><p>miR-22-3p是一种在心血管疾病中具有重要作用的miRNA。它在调节氧化应激、炎症反应和细胞凋亡等多种心血管疾病过程中扮演着关键角色。在心肌梗死损伤模型中，lncRNA<sup> </sup>NORAD可通过靶向miR-22-3p调节哺乳动物雷帕霉素靶蛋白-蛋白激酶B信号传导从而影响心肌细胞凋亡和心肌损伤<sup>［<xref ref-type="bibr" rid="R18">18</xref>］</sup>。此外，Zhou et al<sup>［<xref ref-type="bibr" rid="R19">19</xref>］</sup>发现AMI相关转录物可能作为一种竞争性内源性RNA，通过吸收miR-22-3p来上调死亡相关蛋白激酶2的表达参与扩张型心肌病发病机制的心肌细胞凋亡。本研究中，与CON组对比，AMI患者的血清lncRNA H19的表达水平升高而miR-22-3p的表达水平下降，并且在这种差异表达在AMI不同亚组中仍然存在。现阶段心肌酶学和心电图是AMI诊断和预后的主要评估手段，但有报道<sup>［<xref ref-type="bibr" rid="R7">7</xref>］</sup>证明miR-22-3p的升高较心肌肌钙蛋白更加提前提示，其可能在临床中具有重要的应用价值。另外，本研究表明，血清miR-22-3p含量水平与心肌酶学及心脏射血分数均具有一定的相关性，提示其可能在患者心脏功能学评价中也具有一定意义。在诊断效能方面，本研究ROC曲线分析显示lncRNA H19具有较好的区分AMI与非冠心病患者的能力，而miR-22-3p单独诊断效能有限，但两者联合检测可进一步提高诊断的敏感性。</p><p>目前关于lncRNA H19和miR-22-3p的靶向关系也被相关实验证实。在LPS诱导的肺炎模型中lncRNA H19通过miR-22-3p-NOD样受体热蛋白结构域相关蛋白3轴激活细胞焦亡<sup>［<xref ref-type="bibr" rid="R16">16</xref>］</sup>；在人单核细胞损伤炎性模型中，lncRNA H19 的下调显著抑制白细胞介素-1β、白细胞介素-8和肿瘤坏死因子-α的表达，并且这种调控作用通过miR-22-3p实现<sup>［<xref ref-type="bibr" rid="R17">17</xref>］</sup>。在心肌梗死细胞模型中，LncRNA H19 调节赖氨酸去甲基化酶3A的表达并以miR-22-3p依赖性方式改善心肌梗死后的心肌损伤<sup>［<xref ref-type="bibr" rid="R5">5</xref>］</sup>。这一靶向调控信号通路为理解AMI的分子机制提供了新的视角，并可能为未来的临床诊断和治疗策略的开发提供新的方向。当然本研究仍存在一定局限性：① 本研究为单中心回顾性研究，样本量有限，可能存在选择偏倚；② 未进行多因素回归分析校正性别等潜在混杂因素；③ 仅检测单一时间点表达水平，缺乏动态监测数据；④ 未结合功能实验验证其分子机制。因此，上述结果仍需多中心、大样本前瞻性研究进一步确认。</p><p>综上所述，AMI患者血清中lncRNA H19表达上调，miR-22-3p表达下调，且STEMI患者中上述分子的异常变化较NSTEMI患者更为显著。进一步分析显示，lncRNA H19和miR-22-3p的表达水平与心肌酶、肌钙蛋白及LVEF等临床指标存在相关性，提示二者可能参与AMI的发生发展过程，并在心肌损伤程度及心功能变化中发挥一定作用。这些发现为进一步探讨lncRNA H19和miR-22-3p在AMI病理机制中的调控网络提供了实验依据，可能为未来心肌梗死亚型的分子识别和功能研究提供新的切入点。</p></sec></body><back><ref-list><title>参考文献</title><ref 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