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Melatonin Rescues Influenza A Virus–Induced Cellular Energy Exhaustion via OMA1-OPA1-S in Acute Exacerbation of COPD 在慢性阻塞性肺病急性加重期,褪黑激素通过 OMA1-OPA1-S 挽救甲型流感病毒诱导的细胞能量耗竭。
IF 8.3 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-07-22 DOI: 10.1111/jpi.12991
Yuan-Yuan Wei, Jing-Jing Ye, Da-Wei Zhang, Lei Hu, Hui-Mei Wu, Guang-He Fei

Although rapid progression and a poor prognosis in influenza A virus (IAV) infection–induced acute exacerbation of chronic obstructive pulmonary disease (AECOPD) are frequently associated with metabolic energy disorders, the underlying mechanisms and rescue strategies remain unknown. We herein demonstrated that the level of resting energy expenditure increased significantly in IAV-induced AECOPD patients and that cellular energy exhaustion emerged earlier and more significantly in IAV-infected primary COPD bronchial epithelial (pDHBE) cells. The differentially expressed genes were enriched in the oxidative phosphorylation (OXPHOS) pathway; additionally, we consistently uncovered much earlier ATP exhaustion, more severe mitochondrial structural destruction and dysfunction, and OXPHOS impairment in IAV-inoculated pDHBE cells, and these changes were rescued by melatonin. The level of OMA1-dependent cleavage of OPA1 in the mitochondrial inner membrane and the shift in energy metabolism from OXPHOS to glycolysis were significantly increased in IAV-infected pDHBE cells; however, these changes were rescued by OMA1-siRNA or melatonin further treatment. Collectively, our data revealed that melatonin rescued IAV–induced cellular energy exhaustion via OMA1-OPA1-S to improve the clinical prognosis in COPD. This treatment may serve as a potential therapeutic agent for patients in which AECOPD is induced by IAV.

尽管甲型流感病毒(IAV)感染诱发的慢性阻塞性肺疾病(AECOPD)急性加重的快速进展和不良预后经常与代谢能量紊乱有关,但其潜在机制和救治策略仍然未知。我们在本文中证实,在 IAV 诱导的 AECOPD 患者中,静息能量消耗水平显著增加,而在 IAV 感染的原发性 COPD 支气管上皮细胞(pDHBE)中,细胞能量耗竭出现得更早且更明显。差异表达的基因富集在氧化磷酸化(OXPHOS)通路中;此外,我们不断发现 IAV 感染的 pDHBE 细胞中 ATP 耗竭更早、线粒体结构破坏和功能障碍更严重、OXPHOS 受损更严重,褪黑素可缓解这些变化。在 IAV 感染的 pDHBE 细胞中,线粒体内膜中 OMA1 依赖性裂解 OPA1 的水平和能量代谢从 OXPHOS 到糖酵解的转变显著增加;然而,这些变化在 OMA1-siRNA 或褪黑激素的进一步处理下得到了缓解。总之,我们的数据显示,褪黑激素通过 OMA1-OPA1-S 挽救了 IAV 诱导的细胞能量耗竭,从而改善了慢性阻塞性肺病的临床预后。这种治疗方法可作为一种潜在的治疗药物,用于治疗由 IAV 诱发的 AECOPD 患者。
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引用次数: 0
Phytomelatonin: From Intracellular Signaling to Global Horticulture Market 植物褪黑素:从细胞内信号转导到全球园艺市场
IF 8.3 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-07-19 DOI: 10.1111/jpi.12990
Morteza Soleimani Aghdam, Marino B. Arnao

Melatonin (N-acetyl-5-methoxytryptamine), a well-known mammalian hormone, has been having a great relevance in the Plant World in recent years. Many of its physiological actions in plants are leading to possible features of agronomic interest, especially those related to improvements in tolerance to stressors and in the postharvest life of fruits and vegetables. Thus, through the exogenous application of melatonin or by modifying the endogenous biosynthesis of phytomelatonin, some change can be made in the functional levels of melatonin in tissues and their responses. Also, acting in the respective phytomelatonin biosynthesis enzymes, regulating the expression of tryptophan decarboxylase (TDC), tryptamine 5-hydroxylase (T5H), serotonin N-acetyltransferase (SNAT), N-acetylserotonin O-methyltransferase (ASMT), and caffeic acid O-methyltransferase (COMT), and recently the possible action of deacetylases on some intermediates offers promising opportunities for improving fruits and vegetables in postharvest and its marketability. Other regulators/effectors such as different transcription factors, protein kinases, phosphatases, miRNAs, protein–protein interactions, and some gasotransmitters such as nitric oxide or hydrogen sulfide were also considered in an exhaustive vision. Other interesting aspects such as the role of phytomelatonin in autophagic responses, the posttranslational reprogramming by protein-phosphorylation, ubiquitylation, SUMOylation, PARylation, persulfidation, and nitrosylation described in the phytomelatonin-mediated responses were also discussed, including the relationship of phytomelatonin and several plant hormones, for chilling injury and fungal decay alleviating. The current data about the phytomelatonin receptor in plants (CAND2/PMTR1), the effect of UV-B light and cold storage on the postharvest damage are presented and discussed. All this on the focus of a possible new action in the preservation of the quality of fruits and vegetables.

褪黑素(N-乙酰-5-甲氧基色胺)是一种著名的哺乳动物激素,近年来在植物界具有重要意义。褪黑激素在植物体内的许多生理作用都可能导致农艺学上的兴趣,特别是那些与提高对胁迫的耐受性以及水果和蔬菜的采后寿命有关的作用。因此,通过外源施用褪黑激素或改变植物褪黑激素的内源生物合成,可以在一定程度上改变褪黑激素在组织中的功能水平及其反应。此外,植物褪黑素还能作用于相应的植物褪黑素生物合成酶,调节色氨酸脱羧酶(TDC)、色胺 5-羟化酶(T5H)、血清素 N-乙酰转移酶(SNAT)、N-乙酰基血清素 O-甲基转移酶(ASMT)和咖啡酸 O-甲基转移酶(ASMT)的表达、和咖啡酸 O-甲基转移酶(COMT)的作用,以及最近脱乙酰酶对某些中间产物可能产生的作用,都为改善水果和蔬菜的采后状况及其销路提供了大有可为的机会。其他调控因子/效应因子,如不同的转录因子、蛋白激酶、磷酸酶、miRNAs、蛋白质与蛋白质之间的相互作用,以及一些气体传导物质,如一氧化氮或硫化氢,也在详尽的视野中得到了考虑。此外,还讨论了其他有趣的方面,如植物褪黑激素在自噬反应中的作用,植物褪黑激素介导的反应中描述的蛋白质磷酸化、泛素化、SUMOylation、PARylation、过硫化和亚硝基化等翻译后重新编程,包括植物褪黑激素和几种植物激素在减轻冷害和真菌腐烂方面的关系。会议还介绍并讨论了植物褪黑激素受体(CAND2/PMTR1)、紫外线-B 光和冷藏对收获后损害的影响等方面的最新数据。所有这一切都集中在水果和蔬菜质量保证方面可能采取的新行动上。
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引用次数: 0
Melatonin Ameliorates Atherosclerotic Plaque Vulnerability by Regulating PPARδ-Associated Smooth Muscle Cell Phenotypic Switching 褪黑激素通过调节 PPARδ 相关平滑肌细胞表型转换改善动脉粥样硬化斑块脆弱性
IF 8.3 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-07-09 DOI: 10.1111/jpi.12988
Sy-Jou Chen, Hung-Che Chien, Shih-Hung Tsai, Yu-Sin Jheng, Yi Chen, Po-Shiuan Hsieh, Pi-Fen Tsui, Shu Chien, Min-Chien Tsai

Vulnerable atherosclerotic plaque rupture, the leading cause of fatal atherothrombotic events, is associated with an increased risk of mortality worldwide. Peroxisome proliferator–activated receptor delta (PPARδ) has been shown to modulate vascular smooth muscle cell (SMC) phenotypic switching, and, hence, atherosclerotic plaque stability. Melatonin reportedly plays a beneficial role in cardiovascular diseases; however, the mechanisms underlying improvements in atherosclerotic plaque vulnerability remain unknown. In this study, we assessed the role of melatonin in regulating SMC phenotypic switching and its consequential contribution to the amelioration of atherosclerotic plaque vulnerability and explored the mechanisms underlying this process. We analyzed features of atherosclerotic plaque vulnerability and markers of SMC phenotypic transition in high-cholesterol diet (HCD)–fed apolipoprotein E knockout (ApoE−/−) mice and human aortic SMCs (HASMCs). Melatonin reduced atherosclerotic plaque size and necrotic core area while enhancing collagen content, fibrous cap thickness, and smooth muscle alpha-actin positive cell coverage on the plaque cap, which are all known phenotypic characteristics of vulnerable plaques. In atherosclerotic lesions, melatonin significantly decreased the synthetic SMC phenotype and KLF4 expression and increased the expression of PPARδ, but not PPARα and PPARγ, in HCD-fed ApoE−/− mice. These results were subsequently confirmed in the melatonin-treated HASMCs. Further analysis using PPARδ silencing and immunoprecipitation assays revealed that PPARδ plays a role in the melatonin-induced SMC phenotype switching from synthetic to contractile. Collectively, we provided the first evidence that melatonin mediates its protective effect against plaque destabilization by enhancing PPARδ-mediated SMC phenotypic switching, thereby indicating the potential of melatonin in treating atherosclerosis.

易破裂的动脉粥样硬化斑块是导致致命性动脉粥样硬化血栓事件的主要原因,它与全球死亡风险的增加有关。研究表明,过氧化物酶体增殖激活受体δ(PPARδ)可调节血管平滑肌细胞(SMC)的表型转换,从而影响动脉粥样硬化斑块的稳定性。据报道,褪黑激素在心血管疾病中发挥着有益的作用;然而,动脉粥样硬化斑块脆弱性的改善机制仍不清楚。在这项研究中,我们评估了褪黑激素在调节 SMC 表型转换中的作用及其对改善动脉粥样硬化斑块脆弱性的贡献,并探讨了这一过程的内在机制。我们分析了高胆固醇饮食(HCD)喂养的载脂蛋白E基因敲除(ApoE-/-)小鼠和人类主动脉SMCs(HASMCs)的动脉粥样硬化斑块脆弱性特征和SMC表型转换标记物。褪黑激素能缩小动脉粥样硬化斑块的大小和坏死核心面积,同时提高斑块帽上的胶原蛋白含量、纤维帽厚度和平滑肌α-肌动蛋白阳性细胞覆盖率,这些都是已知的易损斑块的表型特征。在动脉粥样硬化病变中,褪黑素能显著降低合成 SMC 表型和 KLF4 的表达,增加 PPARδ 的表达,但不能增加 PPARα 和 PPARγ 的表达。这些结果随后在褪黑激素处理的 HASMCs 中得到了证实。使用 PPARδ 沉默和免疫沉淀实验进行的进一步分析表明,PPARδ 在褪黑激素诱导的 SMC 表型从合成型向收缩型转换过程中发挥作用。总之,我们首次证明了褪黑激素通过增强PPARδ介导的SMC表型转换对斑块失稳具有保护作用,从而表明了褪黑激素在治疗动脉粥样硬化方面的潜力。
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引用次数: 0
Sleep Deprivation Induces Gut Damage via Ferroptosis 睡眠不足通过铁蛋白沉积诱发肠道损伤
IF 8.3 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-07-08 DOI: 10.1111/jpi.12987
Zi-Jian Zheng, Hai-Yi Zhang, Ya-Lin Hu, Yan Li, Zhi-Hong Wu, Zhi-Peng Li, Dong-Rui Chen, Yang Luo, Xiao-Jing Zhang, Cang Li, Xiao-Yu Wang, Dan Xu, Wei Qiu, Hong-Ping Li, Xiao-Ping Liao, Hao Ren, Jian Sun

Sleep deprivation (SD) has been associated with a plethora of severe pathophysiological syndromes, including gut damage, which recently has been elucidated as an outcome of the accumulation of reactive oxygen species (ROS). However, the spatiotemporal analysis conducted in this study has intriguingly shown that specific events cause harmful damage to the gut, particularly to goblet cells, before the accumulation of lethal ROS. Transcriptomic and metabolomic analyses have identified significant enrichment of metabolites related to ferroptosis in mice suffering from SD. Further analysis revealed that melatonin could rescue the ferroptotic damage in mice by suppressing lipid peroxidation associated with ALOX15 signaling. ALOX15 knockout protected the mice from the serious damage caused by SD-associated ferroptosis. These findings suggest that melatonin and ferroptosis could be targets to prevent devastating gut damage in animals exposed to SD. To sum up, this study is the first report that proposes a noncanonical modulation in SD-induced gut damage via ferroptosis with a clearly elucidated mechanism and highlights the active role of melatonin as a potential target to maximally sustain the state during SD.

睡眠剥夺(SD)与大量严重的病理生理综合征有关,其中包括肠道损伤,最近已被阐明为活性氧(ROS)积累的结果。然而,本研究进行的时空分析有趣地表明,在致命的 ROS 积累之前,特定事件会对肠道,尤其是对腺泡细胞造成有害损害。转录组和代谢组分析发现,在患有 SD 的小鼠体内,与铁变态反应有关的代谢物明显增多。进一步的分析表明,褪黑素可以通过抑制与 ALOX15 信号传导相关的脂质过氧化反应来挽救小鼠的铁氧化损伤。ALOX15 基因敲除可保护小鼠免受 SD 相关铁蛋白沉积症造成的严重损伤。这些研究结果表明,褪黑激素和铁蛋白沉积可作为靶点,防止动物暴露于 SD 后肠道受到毁灭性损伤。总之,本研究是第一份提出通过铁突变对SD诱导的肠道损伤进行非规范调节的报告,其机制已被明确阐明,并强调了褪黑激素作为潜在靶点在最大程度上维持SD期间肠道状态的积极作用。
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引用次数: 0
Melatonin Protects Against Colistin-Induced Intestinal Inflammation and Microbiota Dysbiosis 褪黑素可防止可乐定诱发的肠道炎症和微生物群失调
IF 8.3 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-07-08 DOI: 10.1111/jpi.12989
Yuqian Jia, Tingting Zhang, Mengping He, Bingqing Yang, Zhiqiang Wang, Yuan Liu

Colistin is renowned as a last-resort antibiotic due to the emergence of multidrug-resistant pathogens. However, its potential toxicity significantly hampers its clinical utilization. Melatonin, chemically known as N-acetyl-5-hydroxytryptamine, is an endogenous hormone produced by the pineal gland and possesses diverse biological functions. However, the protective role of melatonin in alleviating antibiotic-induced intestinal inflammation remains unknown. Herein, we reveal that colistin stimulation markedly elevates intestinal inflammatory levels and compromises the gut barrier. In contrast, pretreatment with melatonin safeguards mice against intestinal inflammation and mucosal damage. Microbial diversity analysis indicates that melatonin supplementation prevents a reduction in the abundance of Erysipelotrichales and Bifidobacteriales, as well as an increase in Desulfovibrionales abundance, following colistin exposure. Remarkably, short-chain fatty acids (SCFAs) analysis shows that propanoic acid contributes to the protective effect of melatonin on colistin-induced intestinal inflammation. Furthermore, the protection effects of melatonin and propanoic acid on LPS-induced cellular inflammation in RAW 264.7 cells are confirmed. Mechanistic investigations suggest that intervention with melatonin and propanoic acid can repress the activation of the TLR4 signal and its downstream NF-κB and MAPK signaling pathways, thereby mitigating the toxic effects of colistin. Our work highlights the unappreciated role of melatonin in preventing the potential detrimental effects of colistin on intestinal health and suggests a combined therapeutic strategy to effectively manage intestinal infectious diseases.

由于耐多药病原体的出现,可乐定被誉为最后的抗生素。然而,其潜在的毒性极大地阻碍了它在临床上的应用。褪黑素的化学名称为 N-乙酰-5-羟色胺,是松果体分泌的一种内源性激素,具有多种生物功能。然而,褪黑激素在减轻抗生素诱发的肠道炎症方面的保护作用仍然未知。在本文中,我们发现可乐定刺激会显著升高肠道炎症水平并损害肠道屏障。与此相反,褪黑素可保护小鼠免受肠道炎症和粘膜损伤。微生物多样性分析表明,补充褪黑素可防止小鼠暴露于可乐菌素后Erysipelotrichales和Bifidobacteriales丰度的降低,以及Desulfovibrionales丰度的增加。值得注意的是,短链脂肪酸(SCFAs)分析表明,丙酸有助于褪黑激素对可乐定诱导的肠道炎症产生保护作用。此外,褪黑素和丙酸对 LPS 诱导的 RAW 264.7 细胞炎症的保护作用也得到了证实。机理研究表明,褪黑素和丙酸的干预可以抑制 TLR4 信号及其下游 NF-κB 和 MAPK 信号通路的激活,从而减轻可乐定的毒性作用。我们的研究强调了褪黑激素在预防可乐定对肠道健康的潜在不利影响方面未被重视的作用,并提出了一种有效控制肠道感染性疾病的联合治疗策略。
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引用次数: 0
Mouse Models in Circadian Rhythm and Melatonin Research 昼夜节律和褪黑激素研究中的小鼠模型。
IF 8.3 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-07-04 DOI: 10.1111/jpi.12986
Horst-Werner Korf, Charlotte von Gall

This contribution reviews the role of inbred and transgenic mouse strains for deciphering the mammalian melatoninergic and circadian system. It focusses on the pineal organ as melatonin factory and two major targets of the melatoninergic system, the suprachiasmatic nuclei (SCN) and the hypophysial pars tuberalis (PT). Mammalian pinealocytes sharing molecular characteristics with true pineal and retinal photoreceptors synthesize and secrete melatonin into the blood and cerebrospinal fluid night by night. Notably, neuron-like connections exist between the deep pinealocytes and the habenular/pretectal region suggesting direct pineal-brain communication. Control of melatonin biosynthesis in rodents involves transcriptional regulation including phosphorylation of CREB and upregulation of mPer1. In the SCN, melatonin acts upon MT1 and MT2 receptors. Melatonin is not necessary to maintain the rhythm of the SCN molecular clockwork, but it has distinct effects on the synchronization of the circadian rhythm by light, facilitates re-entrainment of the circadian system to phase advances in the level of the SCN molecular clockwork by acting upon MT2 receptors and plays a stabilizing role in the circadian system as evidenced from locomotor activity recordings. While the effects in the SCN are subtle, melatonin is essential for PT functions. Via the MT1 receptor it drives the PT-intrinsic molecular clockwork and the retrograde and anterograde output pathways controlling seasonal rhythmicity. Although inbred and transgenic mice do not show seasonal reproduction, the pathways from the PT are fully intact if the animals are melatonin proficient. Thus, only melatonin-proficient strains are suited to investigate the circadian and melatoninergic systems.

这篇论文回顾了近交系和转基因小鼠品系在破译哺乳动物褪黑激素能和昼夜节律系统方面的作用。它重点研究了作为褪黑激素工厂的松果体器官以及褪黑激素能系统的两个主要靶点--上丘脑核(SCN)和下丘脑旁(PT)。哺乳动物的松果体细胞与真正的松果体和视网膜感光细胞具有相同的分子特征,每晚合成并分泌褪黑激素到血液和脑脊液中。值得注意的是,深部松果体细胞与视网膜/网膜区域之间存在神经元样连接,这表明松果体与大脑之间存在直接交流。啮齿类动物褪黑激素生物合成的控制涉及转录调控,包括 CREB 磷酸化和 mPer1 的上调。在SCN中,褪黑激素作用于MT1和MT2受体。褪黑激素并不是维持 SCN 分子时钟节律所必需的,但它对光对昼夜节律的同步有明显的影响,通过作用于 MT2 受体,促进昼夜节律系统重新适应 SCN 分子时钟水平的相位变化,并在昼夜节律系统中发挥稳定作用,运动活动记录证明了这一点。虽然褪黑激素对 SCN 的影响是微妙的,但它对 PT 功能至关重要。它通过 MT1 受体驱动昼夜节律内在分子时钟以及控制季节节律的逆行和顺行输出途径。虽然近亲繁殖和转基因小鼠不表现出季节性繁殖,但如果动物缺乏褪黑激素,来自PT的通路则完全完好无损。因此,只有富含褪黑激素的品系才适合研究昼夜节律和褪黑激素能系统。
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引用次数: 0
RETRACTION: Changes in the Expression of Melatonin Receptors Induced by Melatonin Treatment in Hepatocarcinoma HepG2 Cells 回归:褪黑激素治疗诱导的肝癌 HepG2 细胞中褪黑激素受体表达的变化。
IF 8.3 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-06-24 DOI: 10.1111/jpi.12975

RETRACTION: Carbajo-Pescador S, Martín-Renedo J, García-Palomo A, Tuñón MJ, Mauriz JL, González-Gallego J. Changes in the expression of melatonin receptors induced by melatonin treatment in hepatocarcinoma HepG2 cells. Journal of Pineal Research, 2009;47: 330-338. https://doi.org/10.1111/j.1600-079X.2009.00719.x

The above article, published online on 14 October 2009 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Gianluca Tosini, and John Wiley and Sons Ltd. Following publication, concerns were raised by third parties regarding Figure 5. The authors could not provide the original data for this figure, and were unable to provide a satisfactory explanation to resolve the concerns. The retraction has been agreed because of concerns that portions of the figure were duplicated, affecting the interpretation of the data and results presented. The authors disagree with this decision.

撤回:Carbajo-Pescador S、Martín-Renedo J、García-Palomo A、Tuñón MJ、Mauriz JL、González-Gallego J.褪黑激素治疗诱导的肝癌HepG2细胞中褪黑激素受体表达的变化。松果体研究杂志,2009;47:330-338。https://doi.org/10.1111/j.1600-079X.2009.00719.x 上述文章于 2009 年 10 月 14 日在线发表于 Wiley Online Library (wileyonlinelibrary.com),经杂志主编 Gianluca Tosini 和 John Wiley and Sons Ltd.(约翰-威利父子有限公司)协商,该文章已被撤回。文章发表后,第三方对图 5 提出了质疑。作者无法提供该图的原始数据,也无法提供令人满意的解释来消除疑虑。由于担心图中的部分内容被重复,影响对数据和结果的解释,作者同意撤回论文。作者不同意这一决定。
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引用次数: 0
Optimizing the Time and Dose of Melatonin as a Sleep-Promoting Drug: A Systematic Review of Randomized Controlled Trials and Dose−Response Meta-Analysis 优化褪黑素作为促进睡眠药物的使用时间和剂量:随机对照试验的系统回顾与剂量反应元分析》。
IF 10.3 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-06-18 DOI: 10.1111/jpi.12985
Francy Cruz-Sanabria, Simone Bruno, Alessio Crippa, Paolo Frumento, Marco Scarselli, Debra J. Skene, Ugo Faraguna

Previous studies have reported inconsistent results about exogenous melatonin's sleep-promoting effects. A possible explanation relies on the heterogeneity in administration schedule and dose, which might be accountable for differences in treatment efficacy. In this paper, we undertook a systematic review and meta-analysis of double-blind, randomized controlled trials performed on patients with insomnia and healthy volunteers, evaluating the effect of melatonin administration on sleep-related parameters. The standardized mean difference between treatment and placebo groups in terms of sleep onset latency and total sleep time were used as outcomes. Dose−response and meta-regression models were estimated to explore how time of administration, dose, and other treatment-related parameters might affect exogenous melatonin's efficacy. We included 26 randomized controlled trials published between 1987 and 2020, for a total of 1689 observations. Dose−response meta-analysis showed that melatonin gradually reduces sleep onset latency and increases total sleep time, peaking at 4 mg/day. Meta-regression models showed that insomnia status (β = 0.50, p < 0.001) and time between treatment administration and the sleep episode (β = −0.16, p = 0.023) were significant predictors of sleep onset latency, while the time of day (β = −0.086, p < 0.01) was the only significant predictor of total sleep time. Our results suggest that advancing the timing of administration (3 h before the desired bedtime) and increasing the administered dose (4 mg/day), as compared to the exogenous melatonin schedule most used in clinical practice (2 mg 30 min before the desired bedtime), might optimize the efficacy of exogenous melatonin in promoting sleep.

以往的研究对外源性褪黑素促进睡眠效果的研究结果并不一致。一种可能的解释是,给药时间和剂量的不一致性可能是造成疗效差异的原因。在本文中,我们对针对失眠症患者和健康志愿者进行的双盲随机对照试验进行了系统回顾和荟萃分析,评估了服用褪黑素对睡眠相关参数的影响。结果以治疗组和安慰剂组在睡眠开始潜伏期和总睡眠时间方面的标准化平均差异为依据。我们估算了剂量-反应模型和元回归模型,以探讨给药时间、剂量和其他治疗相关参数如何影响外源性褪黑素的疗效。我们纳入了 1987 年至 2020 年间发表的 26 项随机对照试验,共观察到 1689 条数据。剂量-反应荟萃分析表明,褪黑素可逐渐降低睡眠开始潜伏期并增加总睡眠时间,在每天 4 毫克时达到峰值。元回归模型显示,失眠状态(β = 0.50,p
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引用次数: 0
RETRACTION: Melatonin Attenuates Apoptotic Liver Damage in Fulminant Hepatic Failure Induced by the Rabbit Hemorrhagic Disease Virus 返回:褪黑素可减轻兔出血病病毒诱发的暴发性肝衰竭的肝细胞凋亡损伤
IF 10.3 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-06-17 DOI: 10.1111/jpi.12976

RETRACTION: Tuñón MJ, Miguel BS, Crespo I, Jorquera F, Santamaría E, Alvarez M, Prieto J, González-Gallego J. Melatonin attenuates apoptotic liver damage in fulminant hepatic failure induced by the rabbit hemorrhagic disease virus. J Pineal Res 2011;50:38-45. https://doi.org/10.1111/j.1600-079X.2010.00807.x

The above article, published online on 22 October 2010 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Gianluca Tosini, and John Wiley and Sons Ltd. Following publication, concerns were raised by third parties that portions of Figure 4 are duplicated in Figures 4, 2A, and 1B, respectively, of three other articles by the same author group.1-3 The authors provided some of the original data, but these were not sufficient to resolve the concerns, and the authors were unable to provide a satisfactory explanation for the concerns. The retraction has been agreed because of concerns that portions of the figure overlap with the authors' previous articles, affecting the interpretation of the data and results presented. The authors disagree with this decision.

1. Kretzmann NA, Fillmann H, Mauriz JL, Marroni, CA, Marroni N, González-Gallego J, Tuñón MJ. Effects of glutamine on pro-inflammatory gene expression and activation of nuclear factor kappa B and signal transducers and activators of transcription in TNBS-induced colitis. Inflamm Bowel Dis 2008;14:1504-1513. doi:10.1002/ibd.20543

2. Crespo I, García-Mediavilla MV, Gutiérrez B, Sánchez-Campos S, Tuñón MJ, González-Gallego J. A comparison of the effects of kaempferol and quercetin on cytokine-induced pro-inflammatory status of cultured human endothelial cells. Br J Nutr 2008;100(5):968-976. doi:10.1017/S0007114508966083

3. Laliena A, Miguel BS, Crespo I, Alvarez M, González-Gallego J, Tuñón MJ. Melatonin attenuates inflammation and promotes regeneration in rabbits with fulminant hepatitis of viral origin. J Pineal Res 2012;53:270-278. doi:10.1111/j.1600-079X.2012.00995.x

撤回:Melatonin attenuates apoptotic liver damage in fulminant hepatic failure induced by the rabbit hemorrhagic disease virus.J Pineal Res 2011;50:38-45。https://doi.org/10.1111/j.1600-079X.2010.00807.x 上述文章于 2010 年 10 月 22 日在线发表于 Wiley Online Library (wileyonlinelibrary.com),经杂志主编 Gianluca Tosini 和 John Wiley and Sons Ltd.(约翰-威利父子有限公司)协商,该文章已被撤回。文章发表后,第三方提出质疑,认为图 4 的部分内容与同一作者组的另外三篇文章的图 4、图 2A 和图 1B 分别重复。之所以同意撤稿,是因为有人担心该图的部分内容与作者以前的文章重叠,影响了对所提供数据和结果的解释。作者不同意这一决定。1.Kretzmann NA, Fillmann H, Mauriz JL, Marroni, CA, Marroni N, González-Gallego J, Tuñón MJ.谷氨酰胺对 TNBS 诱导的结肠炎中促炎症基因表达以及核因子卡巴 B 和信号转导及转录激活因子激活的影响。Doi:10.1002/ibd.20543 2.Crespo I, García-Mediavilla MV, Gutiérrez B, Sánchez-Campos S, Tuñón MJ, González-Gallego J. 比较山奈酚和槲皮素对细胞因子诱导的培养人内皮细胞促炎状态的影响。doi:10.1017/S0007114508966083 3.Laliena A, Miguel BS, Crespo I, Alvarez M, González-Gallego J, Tuñón MJ.褪黑激素可减轻病毒性暴发性肝炎家兔的炎症反应并促进再生。doi:10.1111/j.1600-079X.2012.00995.x.
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引用次数: 0
RETRACTION: Melatonin Induces Cell Cycle Arrest and Apoptosis in Hepatocarcinoma HepG2 Cell Line 返回:褪黑素诱导肝癌 HepG2 细胞系的细胞周期停滞和细胞凋亡。
IF 10.3 1区 医学 Q1 ENDOCRINOLOGY & METABOLISM Pub Date : 2024-06-17 DOI: 10.1111/jpi.12974

RETRACTION: Martín-Renedo J, Mauriz JL, Jorquera F, Ruiz-Andrés O, González P, González-Gallego J. Melatonin induces cell cycle arrest and apoptosis in hepatocarcinoma HepG2 cell line. J Pineal Res 2008;45:532-540. https://doi.org/10.1111/j.1600-079X.2008.00641.x

The above article, published online on 9 October 2008 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Gianluca Tosini, and John Wiley and Sons Ltd. Following publication, concerns were raised by third parties regarding Figure 5B. The authors could not provide the original data for this figure, and were unable to provide a satisfactory explanation to resolve the concerns. The retraction has been agreed because of concerns that portions of the figure were duplicated, affecting the interpretation of the data and results presented. The authors disagree with this decision.

撤回:Martín-Renedo J, Mauriz JL, Jorquera F, Ruiz-Andrés O, González P, González-Gallego J. Melatonin induces cell cycle arrests and apoptosis in hepatocarcinoma HepG2 cell line.J Pineal Res 2008;45:532-540. https://doi.org/10.1111/j.1600-079X.2008.00641.x 上述文章于 2008 年 10 月 9 日在线发表于 Wiley Online Library (wileyonlinelibrary.com),经杂志主编 Gianluca Tosini 和 John Wiley and Sons Ltd.(约翰-威利父子有限公司)同意,该文章已被撤回。文章发表后,第三方对图 5B 提出了质疑。作者无法提供该图的原始数据,也无法提供令人满意的解释来消除疑虑。由于该图部分内容重复,影响了对数据和结果的解释,因此同意撤稿。作者不同意这一决定。
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引用次数: 0
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Journal of Pineal Research
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