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| 1 | Melatonin enhances radiofrequency-induced NK antitumor immunity,causing cancer metabolism reprogramming and inhibition of multiple pulmonary tumor development显示文摘Surgery is the comm on treatme nt for early lung cancer with multiple pulm onary no dules,but it is often accompanied by the problem of significant malignancy of other nodules in non-therapeutic areas.In this study,we found that a combined treatment of local rad iofreq ue ncy ablati on(RFA)and melatonin(MLT)greatly improved clinical outcomes for early lung cancer patie nts with multiple pulmonary nodules by minimizing lung function injury and reducing the probability of malignant transformation or enlargement of nodules in non-ablated areas.Mechanically,as demonstrated in an associated mouse lung tumor model,RFA not only effectively remove treated tumors but also stimulate antitumor immunity,which could inhibit tumor growth in non-ablated areas.MLT enhanced RFA-stimulated NK activity and exerted synergistic antitumor effects with RFA.Transcriptomics and proteomics analyses of residual tumor tissues revealed enhanced oxidative phosphorylation and reduced acidification as well as hypoxia in the tumor microenvironment,which suggests reprogrammed tumor metabolism after combined treatment with RFA and MLT.Analysis of residual tumor further revealed the depressed activity of MAPK,NF-kappa B,Wnt,and Hedgehog pathways and upregulated P53 pathway in tumors,which was in line with the inhibited tumor growth.Combined RFA and MLT treatment also reversed the Warburg effect and decreased tumor malignancy.These findings thus demonstrated that combined treatment of RFA and MLT effectively inhibited the malignancy of non-ablated nodules and provided an innovative non-invasive strategy for treating early lung tumors with multiple pulmonary nodules.Trial registration:www.chictr.org.cn,identifier ChiCTR2100042695,http://gffzz62a03ee25e6f4a77h0w9xo6p6qkpq66wu.ffgz.tsg.suse.edu.cn/showproj.aspx?proj=120931. | Ming Li Bingjie Hao Menghuan Zhang Russel J.Reiter Shumeng Lin Tiansheng Zheng Xiangyun Chen Yanbei Ren Liduo Yue Baigenzhin Abay Guojie Chen Xiao Xu Yufeng Shi Lihong Fan | 2021 | Signal Transduction and Targeted Therapy2021，6，10： | 6 |
| 2 | Sirtuins, melatonin and circadian rhythms: building a bridge between aging and cancer显示文摘 | BrittneyJung‐Hynes Russel J.Reiter NihalAhmad | 2009 | Journal of Pineal Research2009，，1： | 1 |
| 3 | Melatonin promotes angiogenesis during protection and healing of indomethacin‐induced gastric ulcer: role of matrix metaloproteinase‐2显示文摘 | KrishnenduGanguly Anamika VivekSharma Russel J.Reiter SnehasiktaSwarnakar | 2010 | Journal of Pineal Research2010，，2： | 1 |
| 4 | Melatonin attenuates calpain upregulation, axonal damage and neuronal death in spinal cord injury in rats显示文摘 | SupritiSamantaray Eric A.Sribnick ArabindaDas Varduhi H.Knaryan D. DeniseMatzelle Anil V.Yallapragada Russel J.Reiter Swapan K.Ray Naren L.Banik | 2007 | Journal of Pineal Research2007，，4： | 1 |
| 5 | Beneficial effects of melatonin in protecting against cyclosporine A‐induced cardiotoxicity are receptor mediated显示文摘 | RitaRezzani Luigi F.Rodella FrancescaBonomini SandraTengattini RossellaBianchi Russel J.Reiter | 2006 | Journal of Pineal Research2006，，3： | 1 |
| 6 | Melatonin, the circadian multioscillator system and health: the need for detailed analyses of peripheral melatonin signaling显示文摘 | RüdigerHardeland Juan AntonioMadrid Dun‐XianTan Russel J.Reiter | 2012 | Journal of Pineal Research2012，，2： | 1 |
| 7 | Melatonin decreases cell proliferation and induces melanogenesis in human melanoma SK‐MEL‐1 cells显示文摘 | JavierCabrera GledyNegrín FranciscoEstévez JuanLoro Russel J.Reiter JoséQuintana | 2010 | Journal of Pineal Research2010，，1： | 1 |
| 8 | Melatonin and circadian biology in human cardiovascular disease显示文摘 | AlbertoDominguez‐Rodriguez PedroAbreu‐Gonzalez Juan J.Sanchez‐Sanchez Juan C.Kaski Russel J.Reiter | 2010 | Journal of Pineal Research2010，，1： | 1 |
| 9 | Melatonin as an antibiotic: new insights into the actions of this ubiquitous molecule显示文摘 | Omer FarukTekbas RecaiOgur AhmetKorkmaz AbdullahKilic Russel J.Reiter | 2007 | Journal of Pineal Research2007，，2： | 1 |
| 10 | Melatonin protects against common deletion of mitochondrial DNA‐augmented mitochondrial oxidative stress and apoptosis显示文摘 | Mei‐JieJou Tsung‐IPeng Pai‐ZuYu Shuo‐BinJou Russel J.Reiter Jin‐YiChen Hong‐YuehWu Chih‐ChunChen Lee‐FenHsu | 2007 | Journal of Pineal Research2007，，4： | 1 |
| 11 | Regulation of antioxidant enzymes: a significant role for melatonin显示文摘 | CarmenRodriguez Juan C.Mayo Rosa M.Sainz IsaacAntolín FedericoHerrera VanesaMartín Russel J.Reiter | 2003 | Journal of Pineal Research2003，，1： | 1 |
| 12 | Regulation of antioxidant enzymes: a significant role for melatonin显示文摘 | CarmenRodriguez Juan C.Mayo Rosa M.Sainz IsaacAntolín FedericoHerrera VanesaMartín Russel J.Reiter | 2003 | Journal of Pineal Research2003，，1： | 1 |
| 13 | SGLT2 inhibitor empagliflozin alleviates cardiac remodeling and contractile anomalies in a FUNDC1-dependent manner in experimental Parkinson's disease显示文摘Recent evidence shows a close link between Parkinson's disease(PD)and cardiac dysfunction with limited treatment options.Mitophagy plays a crucial role in the control of mitochondrial quantity,metabolic reprogramming and cell differentiation.Mutation of the mitophagy protein Parkin is directly associated with the onset of PD.Parkin-independent receptor-mediated mitophagy is also documented such as BCL2/adenovirus E1B 19 kDa protein-interacting protein 3(BNIP3)and FUN14 domain containing 1(FUNDC1)for receptor-mediated mitophagy.In this study we investigated cardiac function and mitophagy including FUNDC1 in PD patients and mouse models,and evaluated the therapeutic potential of a SGLT2 inhibitor empagliflozin.MPTP-induced PD model Was established.PD patients and MPTP mice not only displayed pronounced motor defects,but also low plasma FUNDC1 levels,as well as cardiac ultrastructural and geometric anomalies(cardiac atrophy,interstitial fibrosis),functional anomalies(reduced E/A ratio,fractional shortening,ejection fraction,cardiomyocyte contraction)and mitochondrial injury(ultrastructural damage,UcP2,PGC1a,elevated mitochondrial Ca2+uptake proteins MCU and VDAC1,and mitochondrial apoptotic protein calpain),dampened autophagy,FUNDC1 mitophagy and apoptosis.By Gene set enrichment analysis(GSEA),we found overtly altered glucose transmembrane transport in the midbrains of MPTP-treated mice.Intriguingly,administration of SGLT2 inhibitor empagliflozin(10 mg/kg,ip,twice per week for 2 weeks)in MPTP-treated mice significantly ameliorated myocardial anomalies(with exception of VDAC1),but did not reconcile the motor defects or plasma FUNDCi.FUNDC1 global knockout(FUNDC1-/-mice)did not elicit any phenotype on cardiac geometry or function in the absence or presence of MPTP insult,but it nullified empagliflozin-caused cardioprotection against MPTP-induced cardiac anomalies including remodeling(atrophy and fibrosis),contractile dysfunction,Ca2+homeostasis,mitochondrial(including MCU,mitochondrial Ca2+overload,calpain,PARP1)and apoptotic anomalies.In neonatal and adult cardiomyocytes,treatment with PD neurotoxin preformed fibrils of a-synuclein(PFF)caused cytochrome c release and cardiomyocyte mechanical defects.These effects were mitigated by empagliflozin(10μM)or MCU inhibitor Ru360(10μM).MCU activator kaempferol(10μM)or calpain activator dibucaine(500μM)nullified the empagliflozin-induced beneficial effects.These results suggest that empagliflozin protects against PD-induced cardiac anomalies,likely through FUNDC1-mediated regulation of mitochondrial integrity. | Wei Yu Lin Wang Wei-ying Ren Hai-xia Xu Ne N.Wu Dong-hui Yu Russel J.Reiter Wen-liang Zha Qing-dong Guo Jun Ren | 2024 | Acta Pharmacologica Sinica2024，45，1： | 0 |
| 14 | Melatonin,tunneling nanotubes,mesenchymal cells,and tissue regeneration显示文摘Mesenchymal stem cells are multipotent stem cells that reside in many human tissues and organs.Mesenchymal stem cells are widely used in experimental and clinical regenerative medicine due to their capability to transdifferentiate into various lineages.However,when transplanted,they lose part of their multipotency and immunomodulatory properties,and most of them die after injection into the damaged tissue.In this review,we discuss the potential utility of melatonin in preserving mesenchymal stem cells’survival and function after transplantation.Melatonin is a pleiotropic molecule regulating critical cell functions including apoptosis,endoplasmic reticulum stress,and autophagy.Melatonin is also synthesized in the mitochondria where it reduces oxidative stress,the opening of the mitochondrial permeability transition pore and the downstream caspase activation,activates uncoupling proteins,and curtails the proinflammatory response.In addition,recent findings showed that melatonin also promotes the formation of tunneling nanotubes and the transfer of mitochondria between cells through the connecting tubules.As mitochondrial dysfunction is a primary cause of mesenchymal stem cells death and senescence and a critical issue for survival after transplantation,we propose that melatonin by favoring mitochondria functionality and their transfer through tunneling nanotubes from healthy to suffering cells could improve mesenchymal stem cellbased therapy in a large number of diseases for which basic and clinical trials are underway. | Francesca Luchetti Silvia Carloni Maria G.Nasoni Russel J.Reiter Walter Balduini | 2023 | Neural Regeneration Research2023，18，4： | 0 |
| 15 | Promotion of liquid-to-solid phase transition of cGAS by Baicalein suppresses lung tumorigenesis显示文摘Dear Editor,Kras and p53 mutation are among the most common gene mutations in lung cancer,which has both the highest incidence and mortality rate among cancers.1 Kras/p53 mutation also causes mitochondrial dysfunction,which has been implicated to promote the inflammation-to-cancer transition.2 We established a lung adenocarcinoma model by using conditional alleles of KrasLSLG12D/p53flox/flox in mice3 to evaluate the effect of Baicalein(5,6,7-trihydroxyflavone),a principal component of Scutellaria baicalensis in traditional Chinese medicine,4 on the initiation and progression of lung cancer.Cre-mediated expression of KrasG12D and deletion of p53 caused obvious tumor lesions in the lung,which were strongly inhibited by the administration of Baicalein(Fig.1a,b and Supplementary Fig.1a,b),indicating that Baicalein is highly potent in inhibiting the progression of primary lung cancer. | Tiansheng Zheng Haipeng Liu Yifan Hong Yajuan Cao Qing Xia Chengge Qin Ming Li Russel J.Reiter Yidong Bai Lihong Fan | 2023 | Signal Transduction and Targeted Therapy2023，8，4： | 0 |
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