Journal of Pineal Research最新文献

{"title":"Melatonin Rescues Influenza A Virus–Induced Cellular Energy Exhaustion via OMA1-OPA1-S in Acute Exacerbation of COPD","authors":"Yuan-Yuan Wei,&nbsp;Jing-Jing Ye,&nbsp;Da-Wei Zhang,&nbsp;Lei Hu,&nbsp;Hui-Mei Wu,&nbsp;Guang-He Fei","doi":"10.1111/jpi.12991","DOIUrl":"10.1111/jpi.12991","url":null,"abstract":"<div>\u0000 \u0000 <p>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 <i>OMA1</i>-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.</p></div>","PeriodicalId":198,"journal":{"name":"Journal of Pineal Research","volume":"76 5","pages":""},"PeriodicalIF":8.3,"publicationDate":"2024-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141747050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phytomelatonin: From Intracellular Signaling to Global Horticulture Market","authors":"Morteza Soleimani Aghdam,&nbsp;Marino B. Arnao","doi":"10.1111/jpi.12990","DOIUrl":"https://doi.org/10.1111/jpi.12990","url":null,"abstract":"<p>Melatonin (<i>N</i>-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 (<i>TDC</i>), tryptamine 5-hydroxylase (<i>T5H</i>), serotonin <i>N</i>-acetyltransferase (<i>SNAT</i>), <i>N</i>-acetylserotonin <i>O</i>-methyltransferase (<i>ASMT</i>), and caffeic acid <i>O</i>-methyltransferase (<i>COMT</i>), 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.</p>","PeriodicalId":198,"journal":{"name":"Journal of Pineal Research","volume":"76 5","pages":""},"PeriodicalIF":8.3,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jpi.12990","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141730101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Melatonin Ameliorates Atherosclerotic Plaque Vulnerability by Regulating PPARδ-Associated Smooth Muscle Cell Phenotypic Switching","authors":"Sy-Jou Chen,&nbsp;Hung-Che Chien,&nbsp;Shih-Hung Tsai,&nbsp;Yu-Sin Jheng,&nbsp;Yi Chen,&nbsp;Po-Shiuan Hsieh,&nbsp;Pi-Fen Tsui,&nbsp;Shu Chien,&nbsp;Min-Chien Tsai","doi":"10.1111/jpi.12988","DOIUrl":"10.1111/jpi.12988","url":null,"abstract":"<div>\u0000 \u0000 <p>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 (<i>ApoE</i>^−/−) 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 <i>ApoE</i>^−/− 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.</p>\u0000 </div>","PeriodicalId":198,"journal":{"name":"Journal of Pineal Research","volume":"76 5","pages":""},"PeriodicalIF":8.3,"publicationDate":"2024-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141562200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sleep Deprivation Induces Gut Damage via Ferroptosis","authors":"Zi-Jian Zheng,&nbsp;Hai-Yi Zhang,&nbsp;Ya-Lin Hu,&nbsp;Yan Li,&nbsp;Zhi-Hong Wu,&nbsp;Zhi-Peng Li,&nbsp;Dong-Rui Chen,&nbsp;Yang Luo,&nbsp;Xiao-Jing Zhang,&nbsp;Cang Li,&nbsp;Xiao-Yu Wang,&nbsp;Dan Xu,&nbsp;Wei Qiu,&nbsp;Hong-Ping Li,&nbsp;Xiao-Ping Liao,&nbsp;Hao Ren,&nbsp;Jian Sun","doi":"10.1111/jpi.12987","DOIUrl":"10.1111/jpi.12987","url":null,"abstract":"<div>\u0000 \u0000 <p>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.</p>\u0000 </div>","PeriodicalId":198,"journal":{"name":"Journal of Pineal Research","volume":"76 5","pages":""},"PeriodicalIF":8.3,"publicationDate":"2024-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141553826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Melatonin Protects Against Colistin-Induced Intestinal Inflammation and Microbiota Dysbiosis","authors":"Yuqian Jia,&nbsp;Tingting Zhang,&nbsp;Mengping He,&nbsp;Bingqing Yang,&nbsp;Zhiqiang Wang,&nbsp;Yuan Liu","doi":"10.1111/jpi.12989","DOIUrl":"10.1111/jpi.12989","url":null,"abstract":"<div>\u0000 \u0000 <p>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 <i>N</i>-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 <i>Erysipelotrichales</i> and <i>Bifidobacteriales</i>, as well as an increase in <i>Desulfovibrionales</i> 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.</p>\u0000 </div>","PeriodicalId":198,"journal":{"name":"Journal of Pineal Research","volume":"76 5","pages":""},"PeriodicalIF":8.3,"publicationDate":"2024-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141557657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mouse Models in Circadian Rhythm and Melatonin Research","authors":"Horst-Werner Korf,&nbsp;Charlotte von Gall","doi":"10.1111/jpi.12986","DOIUrl":"10.1111/jpi.12986","url":null,"abstract":"<p>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.</p>","PeriodicalId":198,"journal":{"name":"Journal of Pineal Research","volume":"76 5","pages":""},"PeriodicalIF":8.3,"publicationDate":"2024-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jpi.12986","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141533030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: Changes in the Expression of Melatonin Receptors Induced by Melatonin Treatment in Hepatocarcinoma HepG2 Cells","authors":"","doi":"10.1111/jpi.12975","DOIUrl":"10.1111/jpi.12975","url":null,"abstract":"<p><b>RETRACTION:</b> 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. <i>Journal of Pineal Research,</i> 2009;47: 330-338. https://doi.org/10.1111/j.1600-079X.2009.00719.x</p><p>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.</p>","PeriodicalId":198,"journal":{"name":"Journal of Pineal Research","volume":"76 5","pages":""},"PeriodicalIF":8.3,"publicationDate":"2024-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jpi.12975","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141454119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optimizing the Time and Dose of Melatonin as a Sleep-Promoting Drug: A Systematic Review of Randomized Controlled Trials and Dose−Response Meta-Analysis","authors":"Francy Cruz-Sanabria,&nbsp;Simone Bruno,&nbsp;Alessio Crippa,&nbsp;Paolo Frumento,&nbsp;Marco Scarselli,&nbsp;Debra J. Skene,&nbsp;Ugo Faraguna","doi":"10.1111/jpi.12985","DOIUrl":"10.1111/jpi.12985","url":null,"abstract":"<p>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 (<i>β</i> = 0.50, <i>p</i> &lt; 0.001) and time between treatment administration and the sleep episode (<i>β</i> = −0.16, <i>p</i> = 0.023) were significant predictors of sleep onset latency, while the time of day (<i>β</i> = −0.086, <i>p</i> &lt; 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.</p>","PeriodicalId":198,"journal":{"name":"Journal of Pineal Research","volume":"76 5","pages":""},"PeriodicalIF":10.3,"publicationDate":"2024-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jpi.12985","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141417044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: Melatonin Attenuates Apoptotic Liver Damage in Fulminant Hepatic Failure Induced by the Rabbit Hemorrhagic Disease Virus","authors":"","doi":"10.1111/jpi.12976","DOIUrl":"10.1111/jpi.12976","url":null,"abstract":"<p><b>RETRACTION:</b> 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. <i>J Pineal Res</i> 2011;50:38-45. https://doi.org/10.1111/j.1600-079X.2010.00807.x</p><p>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.</p><p>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. <i>Inflamm Bowel Dis</i> 2008;14:1504-1513. doi:10.1002/ibd.20543</p><p>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. <i>Br J Nutr</i> 2008;100(5):968-976. doi:10.1017/S0007114508966083</p><p>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. <i>J Pineal Res</i> 2012;53:270-278. doi:10.1111/j.1600-079X.2012.00995.x</p>","PeriodicalId":198,"journal":{"name":"Journal of Pineal Research","volume":"76 5","pages":""},"PeriodicalIF":10.3,"publicationDate":"2024-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jpi.12976","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141329866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: Melatonin Induces Cell Cycle Arrest and Apoptosis in Hepatocarcinoma HepG2 Cell Line","authors":"","doi":"10.1111/jpi.12974","DOIUrl":"10.1111/jpi.12974","url":null,"abstract":"<p><b>RETRACTION:</b> 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. <i>J Pineal Res</i> 2008;45:532-540. https://doi.org/10.1111/j.1600-079X.2008.00641.x</p><p>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.</p>","PeriodicalId":198,"journal":{"name":"Journal of Pineal Research","volume":"76 5","pages":""},"PeriodicalIF":10.3,"publicationDate":"2024-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jpi.12974","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141329868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}