Redox Biology最新文献

{"title":"Celastrol nanomedicine eye drops restore redox homeostasis and prevents keratoconus progression via PI3K/AKT/AP-1 signaling","authors":"Ruixing Liu,&nbsp;Ruojun Ma,&nbsp;Nan Zhang,&nbsp;Xingchen Geng,&nbsp;Jingguo Li,&nbsp;Lei Zhu,&nbsp;Zhanrong Li","doi":"10.1016/j.redox.2025.103990","DOIUrl":"10.1016/j.redox.2025.103990","url":null,"abstract":"<div><div>Keratoconus (KC) is a progressive corneal disorder primarily driven by oxidative stress, though its precise molecular mechanisms remain incompletely understood, and effective pharmacological treatments are currently lacking. Our proteomic analysis of human KC tissues identified significant oxidative stress signatures and potential PI3K pathway in disease pathogenesis. Subsequent immunohistochemical and Western blot analyses confirmed a pronounced Nox/Nrf-2 redox imbalance - characterized by elevated Nox-4 and Nox-2 and suppressed Nrf-2 - along with activation of the PI3K/AKT/AP-1 signaling axis in KC corneas compared to normal corneas. To model KC-associated oxidative damage <em>in vitro</em>, hydrogen peroxide was used to stimulate rabbit corneal stromal cells. We developed cationic polymeric nanomicelles loaded celastrol (CPNM) to enhance corneal permeability and achieve sustain drug release. In a rabbit KC model, CPNM treatment attenuated corneal curvature progression, increased stromal thickness, and reduced reactive oxygen species (ROS) levels, as assessed by slit-lamp examination, histology, pachymetry, curvature measurements, and biochemical assays. Immunohistochemistry and immunofluorescence further demonstrated that CPNM downregulated PI3K/AKT/AP-1 pathway and restored Nox/Nrf-2 balance in corneal tissues. <em>In vitro,</em> CPNM suppressed ROS, rebalanced the Nox/Nrf-2 system, inhibited PI3K/AKT/AP-1 activation, and reduced matrix metalloproteinase activity. Our findings indicate that CPNM prevents KC progression by concurrently inhibiting oxidative stress <em>via</em> Nox/Nrf-2 balance and suppressing extracellular matrix degradation <em>via</em> PI3K/AKT/AP-1 signaling axis, positioning it as a promising clinical treatment strategy to halt KC progression.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"89 ","pages":"Article 103990"},"PeriodicalIF":11.9,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145822965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Upregulation of PPTC7 in brain microvascular endothelial cell aggravates diabetic cognitive dysfunction by impairing PHB2 mediated mitochondrial function","authors":"Fan Yang ,&nbsp;Pengcheng Pang ,&nbsp;Kang Yang ,&nbsp;Xinyu Niu ,&nbsp;Fang Cheng ,&nbsp;Wei Li","doi":"10.1016/j.redox.2025.103991","DOIUrl":"10.1016/j.redox.2025.103991","url":null,"abstract":"<div><div>Blood-brain barrier impairment (BBB) is the pathological basis of diabetic cognitive dysfunction. Brain microvascular endothelial cells (BMECs) are one of the most mitochondria-rich cell types within the BBB. Mitochondrial dysfunction in BMECs is defined as a pivotal event in diabetic cognitive dysfunction; however, the underlying mechanisms remain poorly understood. Protein phosphatase targeting COQ7 (PPTC7) was screened from RNA-sequencing analysis and its role in regulating mitochondrial function was in both in vitro and in vivo models. PPTC7 expression was predominantly upregulated in BMECs of type 2 diabetes mellitus mice. Genetic manipulations using short hairpin RNA and endothelial-specific adeno-associated virus were applied to investigate the effects of PPTC7 in diabetic cognitive dysfunction. PPTC7 deficiency upregulated mitochondrial oxidative phosphorylation, mitochondrial membrane potential, and mitophagy, but downregulated mitochondrial reactive oxygen species levels in BMECs. Mechanistically, mass spectrometry screening and co-immunoprecipitation assays demonstrated the interaction of PPTC7 with prohibitin 2 (PHB2). PPTC7 disrupts mitochondrial function in BMECs via PHB2 by promoting its ubiquitin-proteasome degradation, which in turn aggravates BBB damage and contributes to diabetic cognitive dysfunction.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"89 ","pages":"Article 103991"},"PeriodicalIF":11.9,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145822964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to “Remote transplantation of human adipose-derived stem cells induces regression of cardiac hypertrophy by regulating the macrophage polarization in spontaneously hypertensive rats” [Redox Biology 27 (2019) 101170]","authors":"Tsung-Ming Lee ,&nbsp;Horng-Jyh Harn ,&nbsp;Tzyy-Wen Chiou ,&nbsp;Ming-Hsi Chuang ,&nbsp;Chun-Hung Chen ,&nbsp;Chi-Hsuan Chuang ,&nbsp;Po-Cheng Lin ,&nbsp;Shinn-Zong Lin","doi":"10.1016/j.redox.2025.103983","DOIUrl":"10.1016/j.redox.2025.103983","url":null,"abstract":"","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"89 ","pages":"Article 103983"},"PeriodicalIF":11.9,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145820528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction notice to “BPTF promotes hepatocellular carcinoma growth by modulating hTERT signaling and cancer stem cell traits” [Redox Biology 20 (2019) 427–441]","authors":"Xinrui Zhao ,&nbsp;Fufu Zheng ,&nbsp;Yizhuo Li ,&nbsp;Jiaojiao Hao ,&nbsp;Zhipeng Tang ,&nbsp;Chunfang Tian ,&nbsp;Qian Yang ,&nbsp;Tianhua Zhu ,&nbsp;Chaoliang Diao ,&nbsp;Changlin Zhang ,&nbsp;Manyu Chen ,&nbsp;Sheng Hu ,&nbsp;Ping Guo ,&nbsp;Lizhi Zhang ,&nbsp;Yina Liao ,&nbsp;Wendan Yu ,&nbsp;Miao Chen ,&nbsp;Lijuan Zou ,&nbsp;Wei Guo ,&nbsp;Wuguo Deng","doi":"10.1016/j.redox.2025.103984","DOIUrl":"10.1016/j.redox.2025.103984","url":null,"abstract":"","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"89 ","pages":"Article 103984"},"PeriodicalIF":11.9,"publicationDate":"2025-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145807931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Redox-active nitroxides enhance cisplatin efficacy against cervical cancer","authors":"Carl P. Soltau ,&nbsp;Debottam Sinha ,&nbsp;Lakshita P. Patil ,&nbsp;Philip M. Moseley ,&nbsp;Cassie L. Rayner ,&nbsp;Nigel L. Barnett ,&nbsp;Derek J. Richard ,&nbsp;Steven E. Bottle ,&nbsp;Ian H. Frazer ,&nbsp;Alexander P. Martyn","doi":"10.1016/j.redox.2025.103989","DOIUrl":"10.1016/j.redox.2025.103989","url":null,"abstract":"<div><div>Cisplatin remains the primary treatment for most cervical cancer cases, though its clinical efficacy is hindered by dose-dependent toxicity and incurring chemoresistance. The overexpression of the glucocorticoid receptor (GR) and cellular redox state is linked to increased resistance to chemotherapy in cervical cancer. This study explores the combinations of novel steroidal and nitroxide-based treatments to improve the efficacy of cisplatin against cervical cancer. Two lead nitroxide-functionalised prednisolone hybrids (<strong>CS91</strong> and <strong>CS187</strong>) were identified for their potent anti-proliferative activity in multiple cervical squamous cell carcinoma (SCC) cell lines. These compounds exhibit comparable anti-proliferative activity to the parent nitroxides, while maintaining GR binding capability. When combined with cisplatin, <strong>CS91</strong> and <strong>CS187</strong> induced a dose-dependent reduction in cell viability across multiple cervical cancer cell lines, which was optimised to preserve above 80 % healthy cell viability but decrease cancer cell viability below 15 %. Mechanistic studies revealed that these compounds raised intracellular reactive oxygen species (ROS) levels, with further enhancement in combination with cisplatin. This combination approach was found to be synergistic, resulting in decreased glutathione (GSH) levels and increased DNA damage compared to cisplatin alone. In summary, nitroxide-based hybrids exhibit potent anti-proliferative effects and potentiate cisplatin efficacy through ROS-mediated mechanisms, offering a promising targeted strategy for cervical cancer treatment.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"89 ","pages":"Article 103989"},"PeriodicalIF":11.9,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145784771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mitochondrial Dynamics and Their Role in the Pathogenesis of Age-Related Macular Degeneration: A Comprehensive Review","authors":"Kai-Yang Chen, Hoi-Chun Chan, Wan-Wan Lin, Chi-Ming Chan","doi":"10.1016/j.redox.2025.103976","DOIUrl":"https://doi.org/10.1016/j.redox.2025.103976","url":null,"abstract":"","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"7 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145796145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unravelling the anti-cancer mechanisms elicited by non-covalent thioredoxin reductase inhibitors for triple negative breast cancer therapy","authors":"Abigail Rullo ,&nbsp;Brenna Flowers ,&nbsp;Keacha Chang ,&nbsp;An Zhang ,&nbsp;Valentina Z. Petukhova ,&nbsp;Luke Harding ,&nbsp;Sammy Y. Aboagye ,&nbsp;Maurizio Bocchetta ,&nbsp;Wei Qiu ,&nbsp;David L. Williams ,&nbsp;Francesco Angelucci ,&nbsp;Pavel A Petukhov ,&nbsp;Irida Kastrati","doi":"10.1016/j.redox.2025.103980","DOIUrl":"10.1016/j.redox.2025.103980","url":null,"abstract":"<div><div>Thioredoxin reductases (cytosolic TXNRD1 and mitochondrial TXNRD2) are antioxidant enzymes often overexpressed in tumors, including triple negative breast cancer (TNBC), making them promising targets for cancer therapy. Inhibiting these enzymes may worsen the already elevated oxidative stress in cancer cells, ultimately leading to cell death through a pro-oxidant mechanism. However, selectively targeting TXNRDs has been challenging due to the traditional reliance on covalent inhibition strategies. Recent studies have identified a druggable allosteric pocket in this enzyme family, paving the way for the development of novel non-covalent inhibitors, referred to as TXNRD(i)s. These inhibitors have been tested in TNBC models and have demonstrated a range of anti-cancer effects.</div><div>To understand the molecular and cellular consequences of TXNRD(i)s, we conducted unbiased transcriptomic analyses and found that the gene expression changes induced by TXNRD(i) treatment closely mirror those resulting from TXNRD1 silencing, reinforcing TXNRD1 as the primary therapeutic target. While TXNRD(i) treatment increases redox stress in TNBC cells, this is not the main driver of the anti-cancer effect. Instead, TXNRD(i)s potently inhibit cell proliferation and induce G1 phase cell cycle arrest. Notably, supplementing cells with exogenous deoxynucleotides restores cell viability, cell cycle progression and partially reverses cell death. These findings indicate that TXNRD(i)s impair ribonucleotide reductase activity and deplete endogenous deoxynucleotide pools as the main mechanism of anti-cancer effects. We further demonstrate that TXNRD(i)s inhibit both TXNRD1 and TXNRD2, and that dual inhibition is more effective in suppressing TNBC cell growth. <em>In vivo</em>, TXNRD(i) treatment significantly impairs TNBC xenograft tumor growth and reduces proliferation-related genes. Collectively, these findings challenge the prevailing paradigm that all TXNRD inhibitors function through a pro-oxidant mechanism, instead highlighting that non-covalent TXNRD(i)s exert their effects by blocking proliferation offering a compelling therapeutic strategy for TNBC and potentially other cancers with elevated TXNRD expression.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"90 ","pages":"Article 103980"},"PeriodicalIF":11.9,"publicationDate":"2025-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145784770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gram-negative bacterial outer membrane proteins and lipopolysaccharides key factors linking chicken coop environment and oxidative stress","authors":"Xuan Liu ,&nbsp;Yue Hao ,&nbsp;Shanlong Tang ,&nbsp;Xiusong Li ,&nbsp;Liang Chen ,&nbsp;Hongfu Zhang","doi":"10.1016/j.redox.2025.103986","DOIUrl":"10.1016/j.redox.2025.103986","url":null,"abstract":"<div><div>High concentrations of particulate matter (PM) in poultry housing act as carriers for microbial aerosols, with Gram-negative bacteria and their outer membrane components—outer membrane proteins (OMPs) and lipopolysaccharide (LPS)—playing pivotal roles in disrupting redox homeostasis. This review systematically examines how OMPs and LPS drive mitochondrial dysfunction and oxidative damage, proposing the “mitochondrial-ROS axis” as an integrative framework to explain their convergent mechanisms. We evaluate evidence that OMPs promote iron dysregulation, target mitochondria, and initiate apoptotic signaling, whereas LPS triggers robust mitochondrial ROS bursts via TLR4/MyD88 and TRAF6-ECSIT pathways, leading to NLRP3 inflammasome activation and pyroptosis. And we further clarify the dynamic conflict between pathogen attack, mediated through the oxidative bursts of OMPs and LPS, and host reductive defenses, including peroxisomal activity, thioredoxin and glutathione systems, and uncoupling proteins. While this axis provides a useful predictive model for anticipating oxidative stress intensity and inflammatory activation, its applicability has notable constraints—such as the context-dependence of ROS in cell-fate decisions and the need for further avian-specific validation of key pathways. This synthesis provides a balanced perspective. Future studies should prioritize avian-specific validation of key pathways and elucidate the temporal dynamics and tissue specificity of ROS responses to inform targeted interventions in poultry health.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"89 ","pages":"Article 103986"},"PeriodicalIF":11.9,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145784772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Physiological oxygen levels reset K+ channel activity in human vascular endothelial cells","authors":"Fan Yang ,&nbsp;Ashia Wheeler-Crawford ,&nbsp;Alan McIntyre ,&nbsp;Giovanni E. Mann ,&nbsp;Joern R. Steinert","doi":"10.1016/j.redox.2025.103981","DOIUrl":"10.1016/j.redox.2025.103981","url":null,"abstract":"<div><div>Human endothelial cells (EC) play a critical role in vascular homeostasis and their function is influenced by oxygen tension. This study investigates for the first time the effects of long-term adaptation (5 days) of two major EC types to physiological oxygen tension (5 kPa) on basal and nitric oxide (NO)-modulated K⁺ channel activities. Whole-cell patch clamp experiments demonstrate that human umbilical vein EC (HUVEC) exhibit larger basal K⁺ outward and smaller inward currents under 5 kPa O₂ compared to standard hyperoxic (18 kPa) culture conditions. Outward currents were potentiated by NO only under hyperoxia. Human cerebral microvascular EC (hCMEC/D3) showed larger outward currents under 5 kPa O₂ which were further potentiated by NO. Pharmacological isolation of different K⁺ currents using tetraethylammonium, TRAM-34 and apamin revealed differential effects in EC adapted to 5 kPa or 18 kPa O₂. Under 5 kPa O₂, both cell types show greater contributions of TEA-sensitive currents and in addition hCMEC/D3 cells exhibit higher proportions of TRAM-34 and apamin-sensitive currents under 5 kPa O₂. In HUVEC, changes in half-activation voltage and hyperpolarized membrane potentials were detected only under hyperoxic conditions following NO exposure, with both cell types exhibiting altered current activation kinetics of outward and inward currents. Notably, expression of KCa3.1, KCa1.1, KCa2.3 and Kir6.1 channels was unaffected by O₂, suggesting that changes in whole-cell currents in both EC types were due to channel modulation. Thus, our findings reveal that physiological O₂ tension shapes the electrophysiological phenotype of human EC by modulating K⁺ channel function and NO responsiveness. The novel insights into the modulation of EC K⁺ channels by O₂ has implications for the regulation of vascular tone and design and use of experimental models <em>in vitro</em> for high throughput drug discovery and clinical translation.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"89 ","pages":"Article 103981"},"PeriodicalIF":11.9,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145784773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resistance-based training improves mitochondrial capacity and redox balance in aging adults, independent of polyphenol supplementation","authors":"Mathias Flensted-Jensen ,&nbsp;Cecilie Moe Weinreich ,&nbsp;Ann-Sofie Kleis-Olsen ,&nbsp;Filip Hansen ,&nbsp;Nadia Stenner Skyggelund ,&nbsp;Jeppe Rahbek Pii ,&nbsp;Ryan Whitlock ,&nbsp;Anders Karlsen ,&nbsp;Arthur Ingersen ,&nbsp;Dace Reihmane ,&nbsp;Daniela Weber ,&nbsp;Tilman Grune ,&nbsp;Olga Pivovarova-Ramich ,&nbsp;Flemming Dela","doi":"10.1016/j.redox.2025.103972","DOIUrl":"10.1016/j.redox.2025.103972","url":null,"abstract":"<div><div>Aging is associated with declines in skeletal muscle function, mitochondrial capacity, and changes in redox balance, which collectively contribute to frailty and chronic disease risk. This study investigated the effects of a 12-week resistance training (RT) program combined with a small dose of high-intensity interval training (HIIT), with or without polyphenol supplementation, on mitochondrial respiratory capacity (MRC) and oxidative stress in middle-aged and older adults (55–70 years). Forty-one participants were randomized to receive either a polyphenol supplement or a placebo for 30 days before the training intervention. Following the training intervention, aerobic capacity, lean mass, and strength improved significantly in both groups. Training also increased MRC in the placebo group but not in the polyphenol group, which displayed higher MRC following the supplementation phase, possibly reflecting either a supplement effect or baseline variation. The training resulted in a 20 % decrease in skeletal muscle H₂O₂ emission across both groups, suggesting enhanced mitochondrial efficiency or antioxidant defenses. However, gene expression of selected antioxidants was unchanged, and plasma oxidative stress markers malondialdehyde (MDA) increased, and 3-nitrotyrosine (3-NT) remained unchanged. Circulating antioxidants showed distinct changes with training, as ascorbic acid increased with training in both groups, while α-tocopherol increased only in the placebo group and β-cryptoxanthin and retinol declined in the polyphenol group, suggesting potential supplement–nutrient interactions. Uric acid increased in both groups, likely reflecting exercise-induced purine turnover. In conclusion, combined RT and HIIT improved mitochondrial bioenergetics and muscle redox balance in middle-aged and older adults, whereas polyphenol supplementation did not augment these adaptations and may have blunted some vitamin-related responses. These findings underscore resistance-based exercise as a potent intervention for maintaining physical and mitochondrial health with age.</div></div>","PeriodicalId":20998,"journal":{"name":"Redox Biology","volume":"89 ","pages":"Article 103972"},"PeriodicalIF":11.9,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145784774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}