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[Research progress on the role of SIRT1 in heart failure]. 【SIRT1在心力衰竭中的作用研究进展】。
Q3 Medicine Pub Date : 2025-04-25 DOI: 10.13294/j.aps.2025.0030
Yang-Ming Zhang, Mai Lyu, Chen-Yang Wu, Yuan-Xi Chen, Guo-Lan Ma, An-Tao Luo

Heart failure (HF) is a common end-stage clinical manifestation of cardiovascular diseases, imposing substantial health-related burdens worldwide. With its high mortality rates and poor long-term prognosis, there is a pressing need for novel therapies. SIRT1, a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, has anti-cardiovascular aging properties and other cardioprotective effects, attracting much research attention in recent years. In addition, SIRT1 plays an important role in HF pathophysiology. This review summarized the roles of SIRT1 and its activators in HF, the changes of SIRT1 gene expression in cardiac tissues from animal models and HF patients, and the current status of clinical trials investigating SIRT1 activators as potential therapies for HF. This will provide new ideas for further exploration of pathological mechanisms and the development of clinical prevention strategies for HF.

心力衰竭(HF)是心血管疾病常见的终末期临床表现,在世界范围内造成了巨大的健康相关负担。由于其高死亡率和较差的长期预后,迫切需要新的治疗方法。SIRT1是一种烟酰胺腺嘌呤二核苷酸(NAD+)依赖的去乙酰化酶,具有抗心血管衰老等心脏保护作用,近年来备受研究关注。此外,SIRT1在HF病理生理中也起着重要作用。本文综述了SIRT1及其激活剂在HF中的作用,动物模型和HF患者心脏组织中SIRT1基因表达的变化,以及SIRT1激活剂作为HF潜在治疗方法的临床试验现状。这将为进一步探索心衰的病理机制和制定临床预防策略提供新的思路。
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引用次数: 0
[NAD+ metabolism in cardiovascular diseases]. [NAD+在心血管疾病中的代谢]。
Q3 Medicine Pub Date : 2025-04-25 DOI: 10.13294/j.aps.2025.0034
Zhao-Zhi Wen, Yi-Hang Yang, Dong Liu, Chong-Xu Shi

Cardiovascular diseases (CVDs) are the leading cause of death worldwide. Nicotinamide adenine dinucleotide (NAD+) is a central and pleiotropic metabolite involved in multiple cellular energy metabolism, such as cell signaling, DNA repair, protein modifications, and so on. Evidence suggests that NAD+ levels decline with age, obesity, and hypertension, which are all significant CVD risk factors. In addition, the therapeutic elevation of NAD+ levels reduces chronic low-grade inflammation, reactivates autophagy and mitochondrial biogenesis, and enhances antioxidation and metabolism in vascular cells of humans with vascular disorders. In preclinical animal models, NAD+ boosting also extends the health span, prevents metabolic syndrome, and decreases blood pressure. Moreover, NAD+ storage by genetic, pharmacological, or natural dietary NAD+-increasing strategies has recently been shown to be effective in improving the pathophysiology of cardiac and vascular health in different animal models and humans. Here, we discuss NAD+-related mechanisms pivotal for vascular health and summarize recent research on NAD+ and its association with vascular health and disease, including hypertension, atherosclerosis, and coronary artery disease. This review also assesses various NAD+ precursors for their clinical efficacy and the efficiency of NAD+ elevation in the prevention or treatment of major CVDs, potentially guiding new therapeutic strategies.

心血管疾病(cvd)是世界范围内死亡的主要原因。烟酰胺腺嘌呤二核苷酸(Nicotinamide adenine dinucleotide, NAD+)是参与细胞信号传导、DNA修复、蛋白质修饰等多种细胞能量代谢的中心多效代谢物。有证据表明,NAD+水平随着年龄、肥胖和高血压而下降,这些都是心血管疾病的重要危险因素。此外,治疗性提高NAD+水平可减少慢性低度炎症,重新激活自噬和线粒体生物发生,并增强血管疾病患者血管细胞的抗氧化和代谢。在临床前动物模型中,提高NAD+还可以延长健康寿命,预防代谢综合征,降低血压。此外,在不同的动物模型和人类中,通过遗传、药理学或天然膳食NAD+增加策略储存NAD+已被证明可有效改善心脏和血管健康的病理生理。在这里,我们讨论了NAD+对血管健康至关重要的相关机制,并概述了NAD+及其与血管健康和疾病(包括高血压、动脉粥样硬化和冠状动脉疾病)的关系的最新研究。本综述还评估了各种NAD+前体在预防或治疗主要心血管疾病中的临床疗效和NAD+升高的效率,可能指导新的治疗策略。
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引用次数: 0
[Acupuncture regulates dynamic flux of Ca2+, Na+, and H2O2 in skeletal muscle injury induced by eccentric exercise in rats]. [针刺调节偏心运动所致大鼠骨骼肌损伤中Ca2+、Na+和H2O2的动态通量]。
Q3 Medicine Pub Date : 2025-02-25
Xue-Lin Zhang, Qian Zhao, Ai-Shan Liu, Ming-Liang Duan, Jing-Jing Ding, Hua Wang

This study aimed to investigate the effects of acupuncture on dynamic changes in Ca2+, Na+, and H2O2 flux following eccentric exercise-induced muscle injury. The total of 324 healthy male Wistar rats were randomly divided into 6 groups: control group (C), eccentric exercise group (E), eccentric exercise with acupuncture group (EA), EA with TRP channel blocker group (EAT), EA with NOX2 blocker group (EAN) and EA with placebo group (EAP). Gastrocnemius muscles were subject to lengthening contractions with percutaneous electrical stimulation, followed by immediate pretreatment with blocking agents. After 30 min, acupuncture needling was administered to the gastrocnemius muscle, and real-time dynamic changes of Ca2+, Na+ and H2O2 flux were measured with non-invasive micro-test technique during the needle retention period, immediately, 3 h, 6 h, and 24 h post-extraction respectively. Results showed that compared with the E group, acupuncture significantly increased net Ca2+ efflux (P < 0.05), extended the period of net Na+ influx, and significantly decreased net H2O2 efflux (P < 0.05). However, these effects were significantly attenuated in the EAT and EAN groups, where excessive net H2O2 efflux was observed (P < 0.001). These findings indicate that acupuncture regulates the dynamic changes of Ca2+, Na+ and H2O2 flux by activating the TRP channels and interacting with NOX2 activity following eccentric exercise-induced skeletal muscle injury.

本研究旨在探讨针刺对偏心运动性肌肉损伤后Ca2+、Na+和H2O2通量动态变化的影响。选取健康雄性Wistar大鼠324只,随机分为6组:对照组(C)、偏心运动组(E)、偏心运动配合针刺组(EA)、偏心运动配合TRP通道阻滞剂组(EAT)、偏心运动配合NOX2阻滞剂组(EAN)、偏心运动配合安慰剂组(EAP)。腓肠肌接受经皮电刺激延长收缩,随后立即用阻断剂预处理。30 min后,针刺腓肠肌,采用无创微测技术,分别测定留针期、即刻、拔针后3 h、6 h、24 h内Ca2+、Na+、H2O2通量的实时动态变化。结果显示,与E组相比,针刺可显著增加净Ca2+外排(P < 0.05),延长净Na+内流时间,显著降低净H2O2外排(P < 0.05)。然而,这些影响在EAT和EAN组显著减弱,观察到过量的H2O2净流出(P < 0.001)。这些结果表明,针刺通过激活TRP通道并与NOX2活性相互作用,调节偏心运动所致骨骼肌损伤后Ca2+、Na+和H2O2通量的动态变化。
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引用次数: 0
[Research progress of nucleus tractus solitarius involved in central regulation of hypertension]. [孤立束核参与高血压中枢调节的研究进展]。
Q3 Medicine Pub Date : 2025-02-25
Yu Tian, Na Li, Yi Zhang, Hong-Jie Wang

The nucleus tractus solitarius (NTS) is the primary brain region for receiving and integrating cardiovascular afferent signals. It plays a crucial role in maintaining balance of autonomic nervous system and regulating blood pressure through cardiovascular reflexes. Neurons within the NTS form complex synaptic connections and interact reciprocally with other brain regions. The NTS regulates autonomic nervous system activity and arterial blood pressure through modulating baroreflex, sympathetic nerve activity, renin-angiotensin-aldosterone system, and oxidative stress. Dysfunctions in NTS activity may contribute to hypertension. Understanding the NTS' role in centrally regulating blood pressure and alterations of neurotransmission or signaling pathways in the NTS may provide rationale for new therapeutic strategies of prevention and treatment. This review summarizes the research findings on autonomic nervous system regulation and arterial blood pressure control by NTS, as well as unresolved questions, in order to provide reference for future investigation.

孤立束核(NTS)是接收和整合心血管传入信号的主要脑区。它在维持自主神经系统平衡和通过心血管反射调节血压方面起着至关重要的作用。NTS内的神经元形成复杂的突触连接,并与大脑其他区域相互作用。NTS通过调节压力反射、交感神经活动、肾素-血管紧张素-醛固酮系统和氧化应激来调节自主神经系统活动和动脉血压。NTS活动功能障碍可能导致高血压。了解NTS在血压集中调节中的作用以及NTS中神经传递或信号通路的改变可能为新的预防和治疗策略提供理论依据。本文综述了NTS在自主神经系统调节和动脉血压控制方面的研究成果及尚未解决的问题,以期为今后的研究提供参考。
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引用次数: 0
[Research progress on the role and mechanism of endothelin-1 in pain]. 内皮素-1在疼痛中的作用及机制研究进展
Q3 Medicine Pub Date : 2025-02-25
Cong-Kun Hu, Hao-Jun You, Jing Lei

Endothelin-1 is a peptide derived from endothelial cells, consisting of 21 amino acid residues. In recent years, research has found that endothelin-1 not only plays a key role in vascular tone regulation but also participates in the occurrence and development of various types of pathological pain, including inflammatory pain, neuropathic pain, and cancer pain. Endothelin-1 binds to its receptors and activates multiple signaling pathways such as protein kinase C, calcium ion channels, and the phosphoinositide pathway, thereby influencing neuronal excitability and nociceptive information transmission. This article briefly reviews the current understanding of the mechanisms and potential roles of endothelin-1 in the development of pain, as well as commonly used endothelin-1 receptor antagonists, aiming to provide clues for better utilizing endothelin-1 and its receptors to alleviate and treat pathological pain.

内皮素-1是一种来源于内皮细胞的肽,由21个氨基酸残基组成。近年来的研究发现,内皮素-1不仅在血管张力调节中起关键作用,而且还参与了各种类型的病理性疼痛的发生和发展,包括炎症性疼痛、神经性疼痛和癌性疼痛。内皮素-1与其受体结合,激活蛋白激酶C、钙离子通道、磷酸肌肽途径等多种信号通路,从而影响神经元的兴奋性和伤害性信息传递。本文简要综述了目前对内皮素-1在疼痛发生发展中的机制和潜在作用的认识,以及常用的内皮素-1受体拮抗剂,旨在为更好地利用内皮素-1及其受体缓解和治疗病理性疼痛提供线索。
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引用次数: 0
[An update on the role of ADAMTS proteoglycanase in female reproductive system]. [ADAMTS蛋白聚糖酶在女性生殖系统中的作用的最新进展]。
Q3 Medicine Pub Date : 2025-02-25
Meng-Die Li, Kang Sun, Wang-Sheng Wang

A disintegrin and metalloproteinase with thrombospondin-like motifs (ADAMTS) represent a diverse family of secreted metalloproteinases, comprising 19 distinct members categorized into five groups based on their substrate specificity: proteoglycanases, procollagen N-peptidases, von Willebrand factor-cleaving protease, cartilage oligomeric matrix proteases and other proteases. Among these, ADAMTS proteoglycanases predominantly target hyalectans, pivotal components in extracellular matrix (ECM) remodeling and inflammation. Dysfunction of ADAMTS proteoglycanases disrupts the structure and function of hyalectans, thereby perturbing ECM homeostasis, resulting in reproduction disorders, including abnormal follicular development, ovulation dysfunction, impaired implantation, placentation and preterm labor. Hence, investigation of the role of ADAMTS proteoglycanases offers valuable insights into the molecular mechanisms underlying the physiological or pathological processes within the female reproductive system, thereby paving the way for innovative strategies in predicting, preventing and treating reproductive system diseases. This review summarizes the recent research advances in the structure and regulation of ADAMTS proteoglycanases and their role in female reproductive system.

具有血小板反应蛋白样基元的崩解素和金属蛋白酶(ADAMTS)代表了一个多样化的分泌金属蛋白酶家族,包括19个不同的成员,根据它们的底物特异性分为五类:蛋白聚糖酶、前胶原n肽酶、血管性血液病因子切割蛋白酶、软骨寡聚基质蛋白酶和其他蛋白酶。其中,ADAMTS蛋白聚糖酶主要靶向透明质素,这是细胞外基质(ECM)重塑和炎症的关键成分。ADAMTS蛋白聚糖酶的功能障碍会破坏透明质体的结构和功能,从而扰乱ECM的内稳态,导致生殖障碍,包括卵泡发育异常、排卵功能障碍、着床、胎盘受损和早产。因此,研究ADAMTS蛋白聚糖酶的作用为研究女性生殖系统生理或病理过程的分子机制提供了有价值的见解,从而为预测、预防和治疗生殖系统疾病的创新策略铺平了道路。本文综述了ADAMTS蛋白聚糖酶的结构、调控及其在女性生殖系统中的作用的最新研究进展。
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引用次数: 0
Research progress on the effects of sedentary behavior and physical activity on diabetes mellitus. 久坐行为与运动对糖尿病影响的研究进展。
Q3 Medicine Pub Date : 2025-02-25
Qi Chen, Chuan-Fen Li, Wen Jing

Diabetes mellitus (DM) has become one of the most serious and common chronic diseases around the world, leading to various complications and a reduction in life expectancy. Increased sedentary behavior (SB) and decreased physical activity (PA) are important contributors to the rising prevalence of DM. This article reviews the research progress on the pathogenesis of DM, the effects of SB and PA on the risk of DM, aiming to explore the influence of different PA intensities, amounts, frequencies, durations and types on the incidence of DM. Research has shown that blood glucose levels tend to increase with the prolongation of SB. Within a certain range, PA intensity and amount are negatively correlated with the risk of DM; Performing PA for more than 3 days per week maintains normal glucose tolerance and lower blood pressure; Engaging in 150-300 min of moderate-intensity exercise or 75-150 min of high-intensity exercise per week reduces the risk of DM; PA during leisure time reduces the risk of DM, while PA during work increases the risk of DM; Both aerobic training and resistance training reduce the risk of DM, and the combination of the two training methods produces better benefits; Various types of exercises, such as cycling, soccer, aerobics, yoga and tai chi, all reduce the risk of DM. In summary, prolonged SB increases the risk of DM, while appropriate PA reduces the risk of DM. As the intensity, amount, and frequency of PA increase, the effect of reducing DM risk becomes more significant. Different exercise methods have different effects on reducing DM risk.

糖尿病(DM)已成为世界上最严重和最常见的慢性疾病之一,导致各种并发症和预期寿命降低。久坐行为(SB)的增加和体力活动(PA)的减少是导致糖尿病患病率上升的重要因素。本文综述了糖尿病发病机制、久坐行为和体力活动对糖尿病风险的影响等方面的研究进展,旨在探讨不同强度、运动量、频率、持续时间和类型对糖尿病发病率的影响。研究表明,随着久坐行为的延长,血糖水平趋于升高。PA强度和数量与DM风险呈负相关;每周进行3天以上的PA治疗可维持正常的葡萄糖耐量和较低的血压;每周进行150-300分钟的中等强度运动或75-150分钟的高强度运动可降低患糖尿病的风险;休闲时间PA降低患DM的风险,工作时间PA增加患DM的风险;有氧训练和抗阻训练都能降低糖尿病的发生风险,两种训练方法结合使用效果更好;各种类型的运动,如骑自行车、足球、有氧运动、瑜伽、太极等,都可以降低糖尿病的风险。综上所述,长时间的SB会增加糖尿病的风险,而适当的PA会降低糖尿病的风险。随着PA的强度、量和频率的增加,降低糖尿病风险的效果更加显著。不同的运动方式对降低糖尿病风险有不同的效果。
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引用次数: 0
[The regulation and mechanism of apolipoprotein A5 on myocardial lipid deposition]. 载脂蛋白A5对心肌脂质沉积的调控及机制研究。
Q3 Medicine Pub Date : 2025-02-25
Xiao-Jie Yang, Jiang Li, Jing-Yuan Chen, Teng-Teng Zhu, Yu-Si Chen, Hai-Hua Qiu, Wen-Jie Chen, Xiao-Qin Luo, Jun Luo
<p><p>The current study aimed to clarify the roles of apolipoprotein A5 (ApoA5) and milk fat globule-epidermal growth factor 8 (Mfge8) in regulating myocardial lipid deposition and the regulatory relationship between them. The serum levels of ApoA5 and Mfge8 in obese and healthy people were compared, and the obesity mouse model induced by the high-fat diet (HFD) was established. In addition, primary cardiomyocytes were purified and identified from the hearts of suckling mice. The 0.8 mmol/L sodium palmitate treatment was used to establish the lipid deposition cardiomyocyte model <i>in vitro</i>. ApoA5-overexpressing adenovirus was used to observe its effects on cardiac function and lipids. The expressions of the fatty acid uptake-related molecules and Mfge8 on transcription or translation levels were detected. Co-immunoprecipitation was used to verify the interaction between ApoA5 and Mfge8 proteins. Immunofluorescence was used to observe the co-localization of Mfge8 protein with ApoA5 or lysosome-associated membrane protein 2 (LAMP2). Recombinant rMfge8 was added to cardiomyocytes to investigate the regulatory mechanism of ApoA5 on Mfge8. The results showed that participants in the simple obesity group had a significant decrease in serum ApoA5 levels (<i>P</i> < 0.05) and a significant increase in Mfge8 levels (<i>P</i> < 0.05) in comparison with the healthy control group. The adenovirus treatment successfully overexpressed ApoA5 in HFD-fed obese mice and palmitic acid-induced lipid deposition cardiomyocytes, respectively. ApoA5 reduced the weight of HFD-fed obese mice (<i>P</i> < 0.05), shortened left ventricular isovolumic relaxation time (IVRT), increased left ventricular ejection fraction (LVEF), and significantly reduced plasma levels of triglycerides (TG) and cholesterol (CHOL) (<i>P</i> < 0.05). In myocardial tissue and cardiomyocytes, the overexpression of ApoA5 significantly reduced the deposition of TG (<i>P</i> < 0.05), transcription of fatty acid translocase (FAT/CD36) (<i>P</i> < 0.05), fatty acid-binding protein (FABP) (<i>P</i> < 0.05), and fatty acid transport protein (FATP) (<i>P</i> < 0.05), and protein expression of Mfge8 (<i>P</i> < 0.05), while the transcription levels of Mfge8 were not significantly altered (<i>P</i> > 0.05). <i>In vitro</i>, the Mfge8 protein was captured using ApoA5 as bait protein, indicating a direct interaction between them. Overexpression of ApoA5 led to an increase in co-localization of Mfge8 with ApoA5 or LAMP2 in cardiomyocytes under lipid deposition status. On this basis, exogenous added recombinant rMfge8 counteracted the improvement of lipid deposition in cardiomyocytes by ApoA5. The above results indicate that the overexpression of ApoA5 can reduce fatty acid uptake in myocardial cells under lipid deposition status by regulating the content and cellular localization of Mfge8 protein, thereby significantly reducing myocardial lipid deposition and improving cardiac diastolic and systolic function
本研究旨在阐明载脂蛋白A5 (ApoA5)和乳脂球-表皮生长因子8 (Mfge8)在心肌脂质沉积中的调节作用及其调控关系。比较肥胖者和健康人血清ApoA5和Mfge8水平,建立高脂饮食诱导的肥胖小鼠模型。此外,我们还从哺乳小鼠的心脏中纯化并鉴定了原代心肌细胞。采用0.8 mmol/L棕榈酸钠处理体外建立脂质沉积心肌细胞模型。用过表达apoa5的腺病毒观察其对心功能和血脂的影响。检测脂肪酸摄取相关分子和Mfge8在转录和翻译水平上的表达。采用共免疫沉淀法验证ApoA5与Mfge8蛋白之间的相互作用。免疫荧光法观察Mfge8蛋白与ApoA5或溶酶体相关膜蛋白2 (LAMP2)的共定位。将重组rMfge8加入心肌细胞,研究ApoA5对Mfge8的调控机制。结果显示,与健康对照组相比,单纯性肥胖组受试者血清ApoA5水平显著降低(P < 0.05), Mfge8水平显著升高(P < 0.05)。腺病毒治疗成功地在hfd喂养的肥胖小鼠和棕榈酸诱导的脂质沉积心肌细胞中过表达ApoA5。ApoA5能降低hfd喂养的肥胖小鼠体重(P < 0.05),缩短左室等容松弛时间(IVRT),提高左室射血分数(LVEF),显著降低血浆甘油三酯(TG)和胆固醇(CHOL)水平(P < 0.05)。在心肌组织和心肌细胞中,ApoA5过表达显著降低TG沉积(P < 0.05)、脂肪酸转位酶(FAT/CD36)转录(P < 0.05)、脂肪酸结合蛋白(FABP)转录(P < 0.05)、脂肪酸转运蛋白(FATP)转录(P < 0.05)和Mfge8蛋白表达(P < 0.05),而Mfge8转录水平无显著改变(P < 0.05)。在体外,以ApoA5作为诱饵蛋白捕获了Mfge8蛋白,表明它们之间存在直接相互作用。ApoA5过表达导致脂质沉积状态下心肌细胞中Mfge8与ApoA5或LAMP2共定位增加。在此基础上,外源性添加重组rMfge8抵消ApoA5对心肌细胞脂质沉积的改善作用。以上结果表明,ApoA5过表达可以通过调节Mfge8蛋白的含量和细胞定位,减少脂质沉积状态下心肌细胞的脂肪酸摄取,从而显著减少心肌脂质沉积,改善心脏舒张和收缩功能。
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引用次数: 0
[Research progress of JAK/STAT signaling pathway in rheumatoid arthritis pain]. JAK/STAT信号通路在类风湿关节炎疼痛中的研究进展
Q3 Medicine Pub Date : 2025-02-25
Zhen-Qiang Liu, Hao-Jun You, Jing Lei

Rheumatoid arthritis (RA) is a common systemic inflammatory autoimmune disease characterized by synovitis and bone destruction. Its clinical characteristics are mainly joint pain, swelling, stiffness and joint deformity. Due to the poor efficacy of both drug and non-drug therapies, RA can significantly impact patients' quality of life and increase personal and socioeconomic burdens. Studies have found that the Janus kinase (JAK)/signal transduction and activator of transcription (STAT) pathway, as classical intracellular signaling pathway, plays an important role in the occurrence and development of connective tissue diseases by regulating inflammation, immunity, and cell differentiation. This article reviews the research progress on the involvement of JAK/STAT signaling pathway in the mechanism of RA pathological pain, in order to provide some reference for understanding the pathogenesis of RA pathological pain and developing specific drug.

类风湿性关节炎(RA)是一种常见的系统性炎症性自身免疫性疾病,以滑膜炎和骨破坏为特征。其临床特征主要为关节疼痛、肿胀、僵硬和关节畸形。由于药物和非药物治疗的疗效较差,RA会显著影响患者的生活质量,增加个人和社会经济负担。研究发现,Janus kinase (JAK)/signal transduction and activator of transcription (STAT)通路作为经典的细胞内信号通路,通过调节炎症、免疫和细胞分化,在结缔组织疾病的发生发展中发挥重要作用。本文就JAK/STAT信号通路参与RA病理性疼痛机制的研究进展进行综述,以期为了解RA病理性疼痛的发病机制和开发特异性药物提供一些参考。
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引用次数: 0
[The historical evolution of Chinese physiology textbooks]. [中国生理学教科书的历史演变]。
Q3 Medicine Pub Date : 2025-02-25
Yan Feng, Xiao Zhai, Xin Wang, Feng Yang, Liang Zhu, Guo-Chao Sun, Ning Wang, Jun Zhang, Jing Xiao, Wei-Wei Liu, You-Fei Guan

This article systematically reviews the characteristics and trends of the writing, editing, publication and promotion of physiology textbooks in China from the late 19th century to the present, focusing on the introduction, development and innovation of Chinese physiology textbooks. The development of physiology textbooks in China is divided into four main stages: the introduction and initial development of physiology textbooks from the late 19th century to 1925; the localization and diversification of textbooks from 1926 to 1949, after the establishment of the Chinese Physiological Society; the exploratory phase of textbook construction after the founding of the People's Republic of China from 1949 to 1976; the formation and innovation of the textbook development process from 1977 to the present, following the restoration of the college entrance examination. For each phase, the article not only records the historical development of physiology textbooks, but also analyzes the evolution of their content, writing styles and the interaction with the social and political contexts. The article summarizes the characteristics and experiences of all these four phases. Special attention is given to the comprehensive statistical analysis of physiology textbooks published since the restoration of the college entrance examination and Economic Reform and Opening-up in 1977, revealing the changes in the number, publication trends and academic features of textbooks during this period. Finally, the article presets the future development of physiology textbooks in China, proposing that textbook writing should integrate aspects such as ideological and political education, medical humanities, basic and clinical medicine, health education, scientific research and international exchange and collaboration. The article also advocates for the application of new technologies and methods, such as artificial intelligence, virtual teaching models and knowledge graphs, to support "personalized learning". This research provides a systematic reference for the study of the history of medical education and offers theoretical support for the future innovation of physiology textbook in China.

本文系统回顾了19世纪末至今中国生理学教科书的编写、编辑、出版和推广的特点和趋势,重点介绍了中国生理学教科书的引进、发展和创新。中国生理学教科书的发展可分为四个主要阶段:19世纪末至1925年生理学教科书的引进和初步发展;1926年至1949年中国生理学会成立后教材的本土化和多样化;建国后1949 - 1976年教材建设的探索阶段;从1977年到现在,随着高考的恢复,教科书的形成和创新的发展过程。对于每个阶段,本文不仅记录了生理学教科书的历史发展,还分析了其内容、写作风格的演变以及与社会政治语境的互动。文章总结了这四个阶段的特点和经验。重点对1977年恢复高考和改革开放以来出版的生理学教科书进行了综合统计分析,揭示了这一时期教科书的数量、出版趋势和学术特征的变化。最后,文章对中国生理学教材的未来发展进行了展望,提出教材编写应从思想政治教育、医学人文、基础与临床、健康教育、科学研究和国际交流与合作等方面进行整合。文章还提倡应用人工智能、虚拟教学模型和知识图谱等新技术和新方法,支持“个性化学习”。本研究为医学教育史的研究提供了系统的参考,并为今后中国生理学教材的创新提供了理论支持。
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生理学报
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