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Article(id=1324050721448010694, tenantId=1146029695717560320, journalId=1227665162245664772, issueId=1324050669933572771, articleNumber=null, orderNo=null, doi=10.20043/j.cnki.MPM.202511265, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1763222400000, receivedDateStr=2025-11-16, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1793607891666, onlineDateStr=2026-11-02, pubDate=1778342400000, pubDateStr=2026-05-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1793607891666, onlineIssueDateStr=2026-11-02, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1793607891666, creator=13701087609, updateTime=1793607891666, updator=13701087609, issue=Issue{id=1324050669933572771, tenantId=1146029695717560320, journalId=1227665162245664772, year='2026', volume='53', issue='9', pageStart='1537', pageEnd='1728', issueExtLink='null', onlineDate='null', pubDate='1778342400000', pubDateStr='2026-05-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1793607879384, creator='13701087609', updateTime=1793670100562, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1324311644528050975, tenantId=1146029695717560320, journalId=1227665162245664772, issueId=1324050669933572771, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1324311644528050976, tenantId=1146029695717560320, journalId=1227665162245664772, issueId=1324050669933572771, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1585, endPage=1589, ext={EN=ArticleExt(id=1324050721670308807, articleId=1324050721448010694, tenantId=1146029695717560320, journalId=1227665162245664772, language=EN, title=Mechanisms by which shift work affects atherosclerosis and intervention strategies, columnId=1228016570660745413, journalTitle=Modern Preventive Medicine, columnName=Environmental and Occupational Health, runingTitle=null, highlight=null, articleAbstract=

Shift work, particularly night shifts and rotating schedules, has become a common working pattern worldwide. However, epidemiological studies indicate that shift work significantly increases the risk of cardiovascular diseases, especially atherosclerosis. By disrupting circadian rhythms, impairing sleep quality, inducing metabolic abnormalities, exacerbating inflammatory responses, causing dyslipidemia, and promoting oxidative stress, shift work facilitates the onset and progression of atherosclerosis (AS). Despite ongoing advances in mechanistic research, the prevention and intervention for AS among shift workers remain inadequate, and health management for this population urgently needs to be strengthened. Therefore, this review synthesizes the current literature to elucidate the mechanisms through which shift work influences AS and to propose effective intervention strategies, with the aim of providing a theoretical basis and practical guidance for cardiovascular health management in shift-working populations.

, authors=Lin-song TIAN1, Hou-rong ZHOU1, 2, authorsList=Lin-song TIAN, Hou-rong ZHOU, authorCompany=null, correspAuthors=Hou-rong ZHOU, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1324050722001658824, articleId=1324050721448010694, tenantId=1146029695717560320, journalId=1227665162245664772, language=CN, title=倒班工作影响动脉粥样硬化的机制与干预对策, columnId=1228016571273113811, journalTitle=现代预防医学, columnName=环境与职业卫生, runingTitle=null, highlight=null, articleAbstract=

倒班工作，尤其是夜班和轮班制，已成为全球普遍的工作模式，但流行病学研究显示，倒班工作显著增加心血管疾病，特别是动脉粥样硬化（atherosclerosis，AS）的风险。倒班通过干扰昼夜节律、影响睡眠质量、诱发代谢异常、加重炎症反应、导致血脂紊乱和促进氧化应激等机制，促进AS的发生与进展。尽管相关机制研究不断深入，倒班工人AS的预防和干预仍不足，健康管理亟待加强。本文通过文献综述，探讨倒班对AS影响的相关机制，并提出有效干预对策，为倒班人群的心血管健康管理提供理论依据和实践指导。

, authors=田林松1, 周厚荣1, 2, authorsList=田林松, 周厚荣, authorCompany=null, correspAuthors=周厚荣, authorNote=

田林松（1998—），男，硕士在读，研究方向：全科医学

, correspAuthorsNote=
周厚荣，E-mail：
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田林松（1998—），男，硕士在读，研究方向：全科医学

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田林松（1998—），男，硕士在读，研究方向：全科医学

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倒班工作影响动脉粥样硬化的机制与干预对策
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田林松 1 , 周厚荣 1, 2
现代预防医学 | 环境与职业卫生 2026,53(9): 1585-1589
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现代预防医学 |环境与职业卫生 2026 , 53 (9) : 1585 -1589
倒班工作影响动脉粥样硬化的机制与干预对策
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田林松1, 周厚荣1, 2
作者信息
  • 1.贵州医科大学，贵州 贵阳 550000
  • 2.贵州省第三人民医院，贵州 贵阳 550008
通讯作者:
周厚荣，E-mail：
作者简介:

田林松（1998—），男，硕士在读，研究方向：全科医学

Mechanisms by which shift work affects atherosclerosis and intervention strategies
Lin-song TIAN1, Hou-rong ZHOU1, 2
Affiliations
  • Guizhou Medical University, Guiyang, Guizhou 550000, China
出版时间: 2026-05-10 doi: 10.20043/j.cnki.MPM.202511265
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倒班工作，尤其是夜班和轮班制，已成为全球普遍的工作模式，但流行病学研究显示，倒班工作显著增加心血管疾病，特别是动脉粥样硬化（atherosclerosis，AS）的风险。倒班通过干扰昼夜节律、影响睡眠质量、诱发代谢异常、加重炎症反应、导致血脂紊乱和促进氧化应激等机制，促进AS的发生与进展。尽管相关机制研究不断深入，倒班工人AS的预防和干预仍不足，健康管理亟待加强。本文通过文献综述，探讨倒班对AS影响的相关机制，并提出有效干预对策，为倒班人群的心血管健康管理提供理论依据和实践指导。

倒班工作  /  动脉粥样硬化  /  昼夜节律  /  炎症反应

Shift work, particularly night shifts and rotating schedules, has become a common working pattern worldwide. However, epidemiological studies indicate that shift work significantly increases the risk of cardiovascular diseases, especially atherosclerosis. By disrupting circadian rhythms, impairing sleep quality, inducing metabolic abnormalities, exacerbating inflammatory responses, causing dyslipidemia, and promoting oxidative stress, shift work facilitates the onset and progression of atherosclerosis (AS). Despite ongoing advances in mechanistic research, the prevention and intervention for AS among shift workers remain inadequate, and health management for this population urgently needs to be strengthened. Therefore, this review synthesizes the current literature to elucidate the mechanisms through which shift work influences AS and to propose effective intervention strategies, with the aim of providing a theoretical basis and practical guidance for cardiovascular health management in shift-working populations.

Shift work  /  Atherosclerosis  /  Circadian rhythm  /  Inflammatory response
田林松, 周厚荣. 倒班工作影响动脉粥样硬化的机制与干预对策. 现代预防医学, 2026 , 53 (9) : 1585 -1589 . DOI: 10.20043/j.cnki.MPM.202511265
Lin-song TIAN, Hou-rong ZHOU. Mechanisms by which shift work affects atherosclerosis and intervention strategies[J]. Modern Preventive Medicine, 2026 , 53 (9) : 1585 -1589 . DOI: 10.20043/j.cnki.MPM.202511265
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倒班工作（包括固定夜班与含夜班的轮转倒班）作为现代社会中不可或缺的职业安排，广泛存在于医疗、交通、制造业等多个行业。随着全球经济和社会结构的变迁，越来越多的劳动者需要适应非传统的工作时间安排。大量流行病学研究表明，倒班工作显著增加了心血管疾病（cardiovascular disease,CVD）发病风险[1-2]，而CVD已成为全球主要的死亡原因之一。动脉粥样硬化（atherosderosis，AS）是CVD的基础性病理过程，其发病机制复杂，涉及血脂代谢紊乱、炎症反应、氧化应激、内皮功能障碍等多重因素[3]。倒班工作通过扰乱生物昼夜节律，影响内分泌、代谢和免疫系统功能，诱发炎症、脂质代谢异常等病理过程，进而加剧CVD的发生与进展[1-2]。
此外，倒班常伴随不规律饮食、缺乏运动、吸烟和酗酒等不良生活方式，进一步增加了心血管风险[4]。倒班工人CVD的发病率显著高于日班工人，并且随着倒班年限延长，风险累积效应明显[5]。尽管倒班工作与AS的关系已得到广泛证实，但其具体机制和有效干预措施仍需进一步研究。本文旨在梳理倒班工作对心血管健康的影响，探讨其机制及干预策略，为高风险人群的健康管理提供理论依据。
在流行病学层面，前瞻性职业队列、横断面研究以及系统综述/荟萃分析的证据总体一致，提示倒班工作与AS及心血管事件风险升高相关[5]。值得注意的是，不同倒班类型与暴露强度可能影响风险大小：以Aragon Workers’ Health Study为代表的影像学研究显示，晨-晚-夜三班轮转（含夜班）与亚临床AS（颈/股动脉斑块或颈动脉内-中膜厚度增厚）关联更为显著，且在校正生活方式与代谢因素后仍然存在[6]。同时，现有证据提示倒班暴露存在累积效应，倒班年限或累积夜班工作量越高，心血管风险越大；剂量-反应荟萃分析显示，每增加5年的夜班/倒班暴露，CVD发生风险进一步上升[2]。总体而言，在评估倒班相关AS风险时，应综合考虑倒班类型（固定夜班 vs.含夜班轮转）及累积暴露指标（倒班年限、夜班频次/累积夜班次数）。
1　倒班工作与昼夜节律紊乱
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1.1　昼夜节律的生理基础
昼夜节律（circadian rhythm）由下丘脑的视交叉上核（suprachiasmatic nucleus, SCN）调控。SCN通过感知光信号调节机体各组织的生物钟，进而控制激素分泌、体温、代谢等生理过程[7]。昼夜节律的分子机制依赖于时钟基因（如CLOCK、BMAL1等）之间的反馈环路，保证生理功能的周期性变化[8]。
正常的昼夜节律有助于维持血压、心率等心血管参数的稳定，调节激素（如褪黑素、糖皮质激素）分泌，对睡眠、觉醒及应激反应起关键作用[9]。一旦昼夜节律受到干扰（如倒班工作、光源暴露、睡眠剥夺），进而会引发激素紊乱、代谢失衡等病理变化，增加心血管和代谢性疾病的风险[7]。因此，深入理解昼夜节律的生理基础，有助于揭示其在动脉硬化等疾病中的作用，为疾病防治提供理论支持。
1.2　倒班工作对昼夜节律的影响
倒班工作可显著干扰人体昼夜节律，导致生物钟错位。昼夜节律主要由SCN统筹调控。固定夜班或含夜班轮转倒班会造成夜间光照暴露增加、睡眠-觉醒与进食时间反转，使内源性生物钟相位发生偏移并降低节律稳定性，进而表现为褪黑素与皮质醇等激素分泌节律紊乱，影响睡眠结构及代谢节律[10]。在分子层面，倒班相关的“时间错配”可导致SCN中枢时钟与肝脏、脂肪、血管等外周组织时钟不同步，使节律性基因表达与下游通路的时间序列失配[11]。
1.3　昼夜节律紊乱与AS的联系
昼夜节律对心血管系统的稳态至关重要，核心生物钟基因（如CLOCK、BMAL1等）调控能量代谢、炎症反应和血管功能等多种生理过程。生物钟基因异常可直接影响血管内皮细胞的代谢和功能。例如，BMAL1缺失的小鼠表现出高脂血症并加速的AS[12]，而CLOCK基因下调会损害内皮细胞的自噬功能，加剧氧化应激和内皮损伤，进而促进斑块的不稳定和进展[13]。
昼夜节律紊乱通过激活免疫炎症、增强巨噬细胞脂质摄取和泡沫细胞形成等机制加速AS的进展[14]。此外，昼夜节律紊乱还通过调控脂质代谢、氧化应激和炎症信号通路（如NF-κB、AMPK等）影响AS的发展[15]。因此，恢复和维持正常的生物钟基因表达对于预防和干预AS具有重要意义。
2　睡眠紊乱与AS
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2.1　倒班工作导致的睡眠障碍
研究表明，倒班工人普遍存在睡眠时长缩短、睡眠质量下降等问题，尤其是夜班工人，常常睡眠不足且睡眠结构紊乱[16]。上述睡眠障碍可加重生物钟错位，使倒班工人在白天难以获得高质量的恢复性睡眠[11]。同时，长期固定夜班或频繁含夜班轮转者的CVD发病率高于日班工人[17]。提示睡眠障碍可能是倒班与心血管不良结局（包括AS）相关的重要中介环节。
2.2　睡眠紊乱促进AS的机制
睡眠障碍是倒班工作常见的健康问题之一，且已被证明能促进AS。睡眠紊乱导致交感神经兴奋，血压升高、心率加快，增加血管壁应力，进而 加速血管内皮损伤和斑块形成[18]。研究发现，睡眠片段化、浅睡眠和夜间觉醒频繁与AS严重程度相关，尤其在糖尿病、下肢 AS 等人群中[19]，睡眠质量差会加速 AS 进展[20]。
睡眠障碍通过激活交感神经系统引起高血压，损伤血管内皮并促进炎症反应和氧化应激，这些因素加速AS的发生与进展[21]。睡眠紊乱还会影响自主神经系统平衡，导致心血管调节紊乱，加剧血管损伤[22]。此外，睡眠片段化增加炎症细胞数量，进一步促进AS的发生[23]。
睡眠障碍与内分泌代谢异常（如胰岛素抵抗、糖脂代谢紊乱）密切相关，这些异常也是AS的危险因素。睡眠质量差还通过影响肠道微生态和代谢物，间接促进血管壁炎症和斑块进展[24]。总之，睡眠障碍通过交感神经兴奋、血压升高、炎症反应、氧化应激和代谢紊乱等多途径共同促进AS进展。改善睡眠质量是预防和延缓AS的重要干预措施。
3　代谢紊乱与血脂异常
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3.1　倒班工作对代谢的影响
倒班工作，已被证实对人体代谢产生不利影响，增加胰岛素抵抗、葡萄糖耐量减退等代谢异常的风险。研究显示，倒班工人发生代谢综合征的风险显著高于日班工人，且这一风险随倒班年限的增加而累积。夜班工作与肥胖、高血压、血糖升高等代谢综合征各组分密切相关，并且夜班次数增多会进一步提高血压风险[25]。此外，倒班还会改变饮食结构和进食时间，引发夜间进食、高热量食物摄入等不规律行为，进一步加剧机体代谢负担。动物实验表明，倒班工作对脂质和葡萄糖代谢有深远影响，维生素D缺乏也是其代谢异常的重要因素[26]。综上所述，倒班工作通过干扰生物钟、激素分泌和饮食行为，显著增加代谢疾病的风险，因此，倒班工人的健康管理应包括饮食干预和优化进食时间。
3.2　血脂异常在AS中的作用
血脂异常，表现为极低密度脂蛋白（very low-density lipoprotein,VLDL）和低密度脂蛋白（low-density lipoprotein,LDL）升高以及高密度脂蛋白（high-density lipoprotein, HDL）降低，是AS发生和发展的核心危险因素。VLDL和LDL的升高促使胆固醇和三酰甘油沉积于血管壁，形成泡沫细胞并逐步发展为AS斑块。氧化型LDL在体内加剧炎症反应、内皮功能障碍及血管平滑肌细胞增殖，加速斑块形成与血管腔狭窄。相反，HDL通过逆向胆固醇转运减少血管壁脂质沉积，并具有抗炎、抗氧化及维持内皮功能的作用。HDL水平下降削弱其保护机制，加速AS进展[27]。长期血脂异常不仅增加斑块形成风险，还与斑块不稳定性及破裂相关，诱发心肌梗死和脑卒中等严重心血管事件[28]。控制血脂异常，特别是降低LDL和VLDL、提高HDL水平，是预防和延缓AS及其并发症的关键措施[27]。
4　炎症反应的激活
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4.1　倒班工作与炎症标志物变化
倒班工作，尤其是夜班和轮班制，已被证实显著影响炎症标志物水平，研究表明倒班工人血液中的C反应蛋白（C-reactive protein，CRP）、高敏感性C反应蛋白（high-sensitivity CRP，hs-CRP）、白细胞介素-6（interleukin-6，IL-6）等炎症因子普遍升高[29]。多项研究显示，倒班工作导致白细胞计数、hs-CRP、TNF-α、IL-1β 等炎症因子升高，诱发慢性低度炎症，进而增加 AS 风险[30-31]。综上所述，倒班工作通过激活免疫系统的炎症反应，增加AS和CVD的发病风险，提示健康管理策略应关注炎症标志物的监测与干预。
4.2　炎症反应促进AS
慢性低度炎症在AS的发生和进展中发挥核心作用。长期的炎症状态激活血管内皮细胞，导致功能障碍并促进黏附分子的表达，进而促进单核细胞的黏附和穿越内皮，进入血管壁，转化为泡沫细胞，加速斑块形成和进展[32]。炎症因子如IL-1β、TNF-α、IL-6等进一步加剧局部炎症，促进泡沫细胞的积聚和斑块核心的扩大[33]。慢性炎症还激活NLRP3炎症小体等通路，形成恶性循环[34]，进一步加速斑块生长和不稳定化，增加其破裂风险，诱发急性心血管事件[32]。内皮细胞功能障碍与氧化应激相互作用，推动AS的进展[35]。因此，针对炎症反应的干预成为预防和治疗AS的重要策略。
5　氧化应激与血管损伤
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5.1　倒班工作诱发氧化应激
倒班工作，尤其是夜班工作，显著扰乱人体的昼夜节律并导致睡眠障碍，这些生理紊乱增加了活性氧的生成，并损害抗氧化防御系统。研究表明，夜班工人氧化应激指标普遍升高，包括DNA损伤、脂质过氧化、活性氧水平增加以及抗氧化能力下降[36]。此外，夜班工人褪黑素分泌受损，进一步削弱抗氧化系统，促进氧化应激。夜班工作还与氧化应激生物标志物呈剂量-反应关系，并影响糖代谢异常[37]。长期夜班工作者体内的氧化DNA损伤标志物持续升高，表明夜班诱发的氧化应激具有累积性[38]。此外，夜班工作通过影响昼夜节律中枢和褪黑素分泌，导致内源性抗氧化物减少，进一步加剧了活性氧的积累[17]。综上所述，倒班工作通过扰乱生物钟和睡眠，增加活性氧生成并损害抗氧化系统，为AS等慢性疾病的发生提供了分子基础。
5.2　氧化应激在AS中的作用
氧化应激在AS的发生与发展中起着核心作用。过量的活性氧损伤血管内皮细胞，破坏血管内皮的完整性，促进LDL氧化形成氧化型LDL，后者被巨噬细胞摄取，形成泡沫细胞，推动AS斑块的形成[39]。活性氧还通过激活核因子κB等信号通路诱发炎症反应，加重血管壁的损伤[35]。
在AS进程中，氧化应激与慢性炎症相互作用，形成恶性循环，增强局部炎症并促进血管平滑肌细胞增殖，进而加速斑块生长和不稳定性增加[40]。氧化应激还促进血管钙化，加速AS进展[41]。活性氧过度产生还会消耗抗氧化系统，加剧氧化损伤[42]。内源性抗氧化因子的表达上调作为代偿性反应有助于减轻损伤[43]。综上所述，氧化应激通过多途径推动AS的发生与进展，干预氧化应激通路有望成为AS防治的新策略。
5.3　倒班相关AS的整合机制框架
倒班工作对AS的影响具有“多通路、网络化”特征。现有研究提示，其上游核心为行为节律与内源性生物钟的持续失配，表现为夜间光照暴露增加、睡眠-觉醒与进食时间后移/反转，从而导致SCN驱动的中枢时钟与肝脏、脂肪、血管等外周时钟发生解耦，节律性基因表达与代谢/免疫通路的时间序列被打乱[8-9]。
在此背景下，倒班相关的节律错位与睡眠紊乱呈双向强化：一方面，昼夜节律相位偏移与褪黑素分泌受抑使恢复性睡眠机会减少并增加睡眠片段化；另一方面，长期睡眠不足又进一步削弱节律稳定性并加重“工作日-休息日”节律摆动[11]。睡眠受损可通过交感神经兴奋与下丘脑-垂体-肾上腺轴激活，造成血压升高与昼夜血压节律异常，并伴随内皮舒张反应受损与促炎状态，从而为血管损伤提供功能学基础[21-22]。
同时，节律错位叠加睡眠受损会改变能量摄入与代谢调控的昼夜时序：夜间进食与饮食结构改变削弱外周组织对进食这一重要授时因子的同步作用，促发胰岛素抵抗、葡萄糖耐量下降及脂代谢异常，进而推动代谢综合征形成[25,44]。代谢紊乱不仅直接增加AS危险因素负荷，还可通过脂毒性与内皮损伤诱发慢性低度炎症。
炎性反应与氧化应激是倒班相关AS进展的关键“放大器”。流行病学与实验研究显示，倒班人群炎症标志物（如CRP、IL-6等）升高，与代谢异常及心血管风险增加相关[30-31]；而慢性炎症可通过黏附分子上调、单核细胞募集、巨噬细胞泡沫化以及炎症小体等途径促进斑块形成与不稳定化[31-34]。与此同时，活性氧生成增加与抗氧化能力下降促进氧化型LDL形成并加重内皮功能障碍，从而与炎症相互促进，推动斑块持续进展[35-37]。
综上，可将倒班相关AS风险概括为“节律错位（上游触发）-睡眠受损（行为与神经内分泌枢纽）-代谢失衡（危险因素汇聚）-炎症/氧化应激（放大环路）”的整合模型。该模型提示：干预策略应优先降低倒班暴露与节律错位强度，并联合睡眠管理与代谢/炎症风险控制，才能更有效阻断从功能紊乱到结构性血管病变的进程。
6　干预措施与健康管理建议
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针对倒班工作相关AS风险的防控，应遵循“源头控制优先、综合干预并行、风险分层管理”的原则，在可行性与成本–效益之间取得平衡。总体而言，减少倒班暴露及其导致的昼夜节律错位是最具群体获益的干预策略，而生活方式管理和医学监测可作为重要补充措施。
6.1　一般性心血管危险因素管理
一般性生活方式干预虽非倒班特异，但对降低AS及心血管事件风险具有明确获益，应作为倒班人群健康管理的基础措施。通过均衡饮食、规律运动、戒烟限酒等方式，可改善代谢状态、降低炎症水平并延缓AS进展[45]。上述措施实施成本低、可及性强，适用于所有倒班人群，应在职业健康管理中常规开展。
6.2　倒班相关的特异性干预策略
从倒班暴露的源头控制与节律再同步角度出发，工作制度优化与节律/睡眠管理是更具针对性的核心优先措施。倒班特异性的风险主要来自昼夜节律错位与睡眠剥夺，因此干预重点应放在“作息-光照-进食时间”的再同步与睡眠管理。建议在排班允许范围内尽量保持相对固定的睡眠窗口，改善睡眠环境（遮光、降噪、适宜温度），并通过个体化睡眠管理减少夜班和轮转导致的睡眠不足与恢复性睡眠缺失[46]；针对倒班相关睡眠障碍，可结合生活方式调整与睡眠卫生教育，以降低心血管并发症发生风险[47]。
在组织管理层面，可通过减少夜班频率、延长班次间休息时间、采用顺时针轮转（早→晚→夜）等方式降低生物节律扰动，并改善工人睡眠质量与心血管风险[48]。在具备条件的单位，可引入AI辅助排班系统以平衡人力需求与休息日安排，提高员工满意度和生活质量[49]。
6.3　倒班人群的医学监测、风险分层与早期筛查
由于医学监测与筛查对资源与成本的需求相对更高，建议在全员基础指标随访的同时，基于风险分层对高危倒班人群实施更强化的检测与影像学评估。在医学监测方面，建议将倒班工人纳入重点随访人群，定期检测血脂、糖化血红蛋白及炎症相关指标（如CRP）以识别早期风险；必要时结合影像学评估进行动态监测，以尽早发现亚临床AS并及时干预[50]。综合采取一般性生活方式管理、倒班相关的排班与睡眠/节律干预以及风险分层筛查，可为倒班工人提供更具针对性的心血管健康管理方案。
7　结论与未来展望
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倒班工作已被大量流行病学与实验研究证实与AS风险增加密切相关。其潜在机制主要涉及昼夜节律紊乱、睡眠障碍、代谢失衡、慢性低度炎症及氧化应激等多条相互交织的通路，这些因素共同促进血管内皮功能障碍和AS的发生与进展。现有证据提示，长期或高强度倒班暴露人群面临更高的心血管风险，且该风险具有一定的累积效应。
针对倒班相关AS风险的防控，应在职业健康管理中加强对倒班人群的系统评估与综合干预，包括优化排班制度以减少昼夜节律错位，改善睡眠管理，强化生活方式与代谢危险因素控制，并对高危个体实施针对性的医学监测与早期干预。
未来研究有必要在以下方面进一步深化：第一，推动倒班暴露评估的标准化与精细化，结合客观排班记录和亚临床AS指标开展多中心前瞻性研究；第二，加强机制研究的整合与转化，在人体研究中同步评估节律、睡眠、代谢及炎症相关指标，以明确关键致病通路；第三，开展基于真实倒班场景的干预研究，系统评价排班优化及节律与睡眠干预对心血管结局的影响，为倒班人群的精准健康管理提供循证依据。
基金
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  • 贵州省科技厅科技支撑计划项目(黔科合支撑[2022]一般195)
文献
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2026年第53卷第9期
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doi: 10.20043/j.cnki.MPM.202511265
  • 接收时间：2025-11-16
  • 首发时间：2026-11-02
  • 出版时间：2026-05-10
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  • 收稿日期：2025-11-16
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贵州省科技厅科技支撑计划项目(黔科合支撑[2022]一般195)
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    1.贵州医科大学，贵州 贵阳 550000
    2.贵州省第三人民医院，贵州 贵阳 550008

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Number of
species		 占总种数比例
Percentage of
total species (%)		 属
Genus		 种数
Number of
species		 占总种数比例
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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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