Biochimica et biophysica acta. Molecular and cell biology of lipids最新文献

{"title":"Curcumol ameliorates high-fat diet-induced hepatic fibrosis via dual regulation of FXR-CREB and Rab18-mediated hepatic stellate cell lipophagy","authors":"Na Wei ,&nbsp;Wanyu Feng ,&nbsp;Meijun Pan ,&nbsp;Xinyi Xu ,&nbsp;Shuguo Zheng ,&nbsp;Huanhuan Jin","doi":"10.1016/j.bbalip.2025.159710","DOIUrl":"10.1016/j.bbalip.2025.159710","url":null,"abstract":"<div><div>Curcumol, a bioactive constituent derived from <em>Rhizoma Curcumae</em> roots, possesses anti-inflammatory and anti-viral properties. This study investigated its therapeutic effects on lipophagy in hepatic stellate cells (HSCs) and lipid accumulation in hepatocytes within a model of high-fat diet-induced hepatic fibrosis, along with the underlying molecular mechanisms. Initially, curcumol treatment significantly attenuated lipid droplets (LDs) degradation and suppressed HSC activation, effects potentially associated with the inhibition of lipophagy. These outcomes were partially reversed by Rab18 overexpression, which modulates the autophagy-lysosomal pathway. Moreover, the ameliorative effect of curcumol on choline-deficient, L-amino acid-defined, 45 % high-fat diet (CDAHFD)-induced hepatic pathology was partially abolished upon Rab18 overexpression in mice. Importantly, curcumol promoted Farnesoid X receptor (FXR) expression, which inhibited the CREB/TORC2 interaction, thereby further suppressing LC3B expression and activation in LX2 cells. Additionally, curcumol impeded LD expansion and reduced lipid accumulation in palmitic acid (PA)-treated BNL-CL.2 cells and hepatocytes from CDAHFD-fed mice by inhibiting LD–endoplasmic reticulum (ER) contact formation, which could be reversed by Rab18 overexpression. In conclusion, curcumol inhibits HSC lipophagy by downregulating Rab18-mediated LD–autophagosome formation and enhancing the FXR–CREB interaction. Furthermore, it ameliorates hepatocyte lipid accumulation in fibrotic livers by disrupting Rab18-dependent LD–ER contacts. These findings underscore the therapeutic potential of curcumol in the treatment of HFD-induced hepatic fibrosis.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1871 2","pages":"Article 159710"},"PeriodicalIF":3.3,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145751467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MiR-424-3p suppresses adipogenesis via HNRNPA0 targeting and p53-mediated ferroptosis","authors":"Meng Li ,&nbsp;Yuqi Ye ,&nbsp;Shasha Lin ,&nbsp;Hanchen Jiang ,&nbsp;Dawei Zhang ,&nbsp;Jin Zhang","doi":"10.1016/j.bbalip.2025.159712","DOIUrl":"10.1016/j.bbalip.2025.159712","url":null,"abstract":"<div><div>MicroRNAs (miRNAs), a class of non-coding small RNAs, play critical roles in regulating adipocyte biology, including differentiation, proliferation, and lipid metabolism. This study investigates the role of miR-424-3p in adipogenesis. MiR-424-3p expression is dynamically upregulated during adipocyte differentiation. Functional analyses demonstrate that miR-424-3p overexpression suppresses lipid droplet accumulation and coordinately inhibits both anabolic (PPARγ, C/EBPα) and catabolic (ATGL, HSL) pathways; these effects are reversed by co-treatment with a miR-424-3p inhibitor. Lipidomic analysis reveals that miR-424-3p mediates membrane phospholipid remodeling, with significant changes predominantly in glycerophospholipids and sphingolipids, among which PE, PC, and LPE are the major affected species. Together with pathway enrichment analysis, increased lipid reactive oxygen species (ROS) levels, decreased glutathione (GSH) levels, and unaltered cell viability, these results collectively indicate that miR-424-3p may trigger ferroptosis signaling. Mechanistically, we demonstrate that miR-424-3p targets HNRNPA0, thereby upregulating p53 and suppressing ferroptosis inhibitors (SLC7A11, GPX4). HNRNPA0 overexpression reverses these phenotypes, restoring adipocyte metabolism and lipid storage capacity. Our findings establish miR-424-3p as an epigenetic regulator of adipose homeostasis via the HNRNPA0-p53-ferroptosis axis, which constrains lipid accumulation in 3T3-L1 cells. The evolutionary conservation of this mechanism across lipogenically active species highlights its potential as a therapeutic target for obesity-related metabolic disorders.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1871 2","pages":"Article 159712"},"PeriodicalIF":3.3,"publicationDate":"2025-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145740748","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Celebrating 50 years of insight-Bob Michell's legacy in phosphoinositide signalling.","authors":"","doi":"10.1016/j.bbalip.2025.159709","DOIUrl":"10.1016/j.bbalip.2025.159709","url":null,"abstract":"","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":" ","pages":"159709"},"PeriodicalIF":3.3,"publicationDate":"2025-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145699651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Roles in physiology and disease of the inositol phosphatase synaptojanin 1","authors":"Pietro De Camilli","doi":"10.1016/j.bbalip.2025.159708","DOIUrl":"10.1016/j.bbalip.2025.159708","url":null,"abstract":"<div><div>Synaptojanin 1 (Synj1) is a protein highly enriched in the nervous system which comprises tandemly arranged inositol 4-phosphatase and 5-phosphatase domains. Since its discovery as a synaptically enriched binding partner of SH3 domain containing proteins, Synj1 has been shown to be a key player in synaptic vesicle recycling via its property to couple the endocytic reaction to dephosphorylation of PI(4,5)P₂, a determinant of plasma membrane identity. Beyond its well established role in synaptic vesicle traffic, Synj1 has housekeeping roles at the interface of endocytosis, receptor signaling and regulation of actin nucleation. It is essential for postnatal life, while partial loss-of-function mutations are responsible for early-onset Parkinsonism and epilepsy. Conversely Synj1 overexpression, such as due to gene duplication in Down syndrome, may also have a pathogenic role. Here I review current knowledge about Synj1's molecular and physiological functions and the role of its dysfunction in disease.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1871 2","pages":"Article 159708"},"PeriodicalIF":3.3,"publicationDate":"2025-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145660148","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phosphoinositides at 50: From minor lipids to master organizers of polarity","authors":"Ama Gassama-Diagne","doi":"10.1016/j.bbalip.2025.159707","DOIUrl":"10.1016/j.bbalip.2025.159707","url":null,"abstract":"<div><div>Phosphoinositides (PIs) have been at the center of cell signaling and membrane biology since Michell's proposal of the PI-cycle in 1975. Over the past fifty years, these quantitatively minor lipids have emerged as versatile molecular organizers, defining membrane identity, generating spatial cues, coordinating cytoskeletal dynamics and thus playing pivotal role in polarity. Studies in yeast, amoebae, and neutrophils demonstrated how localized PI pools regulate polarity and chemotaxis, providing a conceptual advance to tissue-level organization. In epithelia, PIs now stand as central determinants of apico-basal polarity and lumen morphogenesis through their cooperation with Rho GTPases, polarity complexes, and septins. This review highlights how these lipids shape our understanding of membrane dynamics and epithelial tissue organization. To conclude, this review underscores how alterations in the activities of these polarity regulators lead to abnormal epithelial morphogenesis and severe diseases such as cancer.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1871 2","pages":"Article 159707"},"PeriodicalIF":3.3,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145548064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Subcellular Cartography of the Phosphoinositide Multiverse","authors":"Morgan M.C. Ricci ,&nbsp;Claire C. Weckerly ,&nbsp;Gerald R.V. Hammond","doi":"10.1016/j.bbalip.2025.159706","DOIUrl":"10.1016/j.bbalip.2025.159706","url":null,"abstract":"<div><div>Phosphoinositides (PPIn) are low-abundance phospholipids that define membrane identity and direct compartment-specific signaling across eukaryotic cells. Marking fifty years since Michell's seminal 1975 review, we re-evaluate how the subcellular localization of these lipids informs their function. Using a historical and mechanistic framework, we survey evidence for the steady-state distribution of all eight PPIn species and their key precursor, phosphatidic acid, emphasizing live-cell biosensor studies and kinase localization. We conclude that PI(4,5)P₂ and PIP₃ signaling remain largely confined to the plasma membrane, whereas PI4P and PI3P occupy distinct but complementary domains of the Golgi and endosomal systems, and PI(3,5)P₂ marks specialized late endosomal compartments. Together, these patterns reveal PPIn as spatial rather than purely temporal signaling molecules—an ATP-derived currency maintaining the ordered heterogeneity of eukaryotic membranes. Understanding how these pathways self-regulate will define the next generation of phosphoinositide biology.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1871 2","pages":"Article 159706"},"PeriodicalIF":3.3,"publicationDate":"2025-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145548097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ATGL-mediated lipolysis is essential for myocellular mitochondrial function, mitochondria-lipid droplet interaction and mitochondrial network connectivity","authors":"Anne Gemmink ,&nbsp;Tineke van de Weijer ,&nbsp;Gert Schaart ,&nbsp;Gernot F. Grabner ,&nbsp;Esther Kornips ,&nbsp;Kèvin Knoops ,&nbsp;Rudolf Zechner ,&nbsp;Martina Schweiger ,&nbsp;Matthijs K.C. Hesselink","doi":"10.1016/j.bbalip.2025.159703","DOIUrl":"10.1016/j.bbalip.2025.159703","url":null,"abstract":"<div><div>Defects in Adipose tissue TriGlyceride Lipase (ATGL)-mediated myocellular lipid droplet (LD) lipolysis results in mitochondrial dysfunction of unknown origin, which can be rescued by PPAR agonists. Here we examine if ATGL-mediated lipolysis is required to maintain mitochondrial network connectivity and function. Moreover, we explored if the functional implications of ATGL deficiency for mitochondrial network dynamics and function can be alleviated by promoting PPARα and/or PPARδ transcriptional activity. To this end, we cultured human primary myotubes from patients with neutral lipid storage disease with myopathy (NLSDM), a rare metabolic disorder caused by a mutation in the gene encoding for ATGL. These myotubes possess dysfunctional ATGL and compromised LD lipolysis. In addition, mitochondria-LD contact, mitochondrial network connectivity, and mitochondrial membrane potential were affected. Using a humanized ATGL inhibitor in myotubes (cultured form healthy donors) revealed similar results. Upon stimulating PPARδ transcriptional activity, mitochondrial respiration improved by more than 50 % in human primary myotubes from healthy lean individuals. This increase in respiration was dampened in myotubes with dysfunctional ATGL. Stimulation of PPARδ transcriptional activity had no effect on mitochondria-LD contacts, mitochondrial network connectivity, and mitochondrial membrane potential. Our results demonstrate that dysfunctional ATGL results in compromised mitochondrial-LD contacts and mitochondrial network connectivity, and that functional ATGL is required to improve mitochondrial respiratory capacity upon stimulation of PPARδ transcriptional activity.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1871 1","pages":"Article 159703"},"PeriodicalIF":3.3,"publicationDate":"2025-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145501933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Melatonin ameliorates ox-LDL-induced lipid accumulation and enhances ABCA1 expression in VSMCs via inhibition of the TRPV1-Ca2+-calpain signaling pathway","authors":"Yuehong Tang ,&nbsp;Yujiao Peng ,&nbsp;Yaling Zhang ,&nbsp;Wenjuan Tong ,&nbsp;Shaowei Sun","doi":"10.1016/j.bbalip.2025.159704","DOIUrl":"10.1016/j.bbalip.2025.159704","url":null,"abstract":"<div><div>Oxidized low-density lipoprotein (ox-LDL) has been shown to induce significant lipid accumulation and disrupt cholesterol homeostasis in vascular smooth muscle cells (VSMCs), which may contribute to the development of atherosclerosis (AS). In this study, we investigated the effects of ox-LDL on lipid accumulation, and the expression of key proteins involved in cholesterol transport, such as ATP-binding cassette transporter A family member 1 (ABCA1). Our results demonstrated that ox-LDL treatment led to a concentration-dependent increase in intracellular lipid content, as evidenced by Oil Red O and BODIPY staining. Additionally, ox-LDL elevated intracellular calcium (Ca²⁺) levels and activated the Ca²⁺-Calpain signaling pathway, which in turn suppressed the expression of ABCA1, a critical protein responsible for cholesterol efflux. We further explored the therapeutic potential of melatonin (MLT) in mitigating the harmful effects of ox-LDL. Treatment with MLT significantly improved cell viability and reduced lipid accumulation in VSMC. Moreover, MLT, along with specific inhibitors of the TRPV1-Ca²⁺-Calpain pathway (Capsazepine, EGTA, and Calpeptin), successfully lowered intracellular Ca²⁺ levels and calpain activity, while restoring ABCA1 expression at protein levels but not mRNA. These findings suggest that MLT exerts a protective effect by inhibiting the TRPV1-Ca²⁺-Calpain signaling pathway, thereby promoting cholesterol efflux and reducing lipid accumulation in VSMCs. To validate these findings in vivo, ApoE^−/− mice were fed a high-fat diet (HFD) for 12 weeks to induce atherosclerotic lesions, with MLT administered via intraperitoneal injection during the final 6 weeks. Histological analyses of the aortic root revealed that MLT treatment significantly reduced atherosclerotic plaque areas compared to untreated HFD-fed mice. Furthermore, Western blot analyses demonstrated that MLT increased ABCA1 expression and decreased TRPV1 expression in aortic tissues, aligning with our in vitro observations. In conclusion, our study highlights the role of the TRPV1-Ca²⁺-Calpain signaling pathway in ox-LDL-induced lipid dysregulation and identifies MLT as a potential therapeutic agent for reversing these effects, offering new insights into the molecular mechanisms underlying lipid accumulation in VSMCs.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1871 1","pages":"Article 159704"},"PeriodicalIF":3.3,"publicationDate":"2025-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145487656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sphinganine-induced lysosomal membrane permeabilization: Interplay with subcellular oxidative levels","authors":"Guodong Cheng ,&nbsp;Changxi Qi ,&nbsp;Huiling Xu ,&nbsp;Xiaozhou Wang ,&nbsp;Muzi Li ,&nbsp;Huahua Chen ,&nbsp;Pimiao Zheng ,&nbsp;Yongxia Liu ,&nbsp;Jianzhu Liu ,&nbsp;Xiaona Zhao","doi":"10.1016/j.bbalip.2025.159705","DOIUrl":"10.1016/j.bbalip.2025.159705","url":null,"abstract":"<div><div>Sphinganine (SA), a fundamental sphingolipid whose cytotoxicity remains incompletely characterized, has received less attention compared to other sphingoid bases. Here, we demonstrate that SA predominantly triggers cell death via lysosomal membrane permeabilization (LMP) resulting from pH dysregulation and osmotic imbalance, rather than through direct ROS-mediated mechanisms, although mitochondrial ROS contribute to oxidative stress. SA-induced mitochondrial fragmentation significantly increased hydrogen peroxide levels in both the mitochondrial matrix and intermembrane space (IMS). Strikingly, lysosomes exhibited spatial colocalization with elevated hydrogen peroxide microdomains under SA exposure, suggesting a redox-dependent mechanism governing organelle repositioning. The cysteine protease inhibitor E64D attenuated SA-induced apoptosis through suppressing cathepsin B/L release, confirming lysosomal membrane permeabilization as an executor of apoptotic signaling. These findings unveil SA's dual-targeting organelle toxicity mechanism. Our study not only elucidates key aspects of sphingolipid-mediated cytotoxicity but also provides therapeutic rationale for counteracting fumonisin B1 (FB1)-induced pathologies and related sphingolipid disorders, potentially through lysosomal stabilization or targeted ROS modulation.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1871 1","pages":"Article 159705"},"PeriodicalIF":3.3,"publicationDate":"2025-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145487152","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional analysis and regulation mechanism of FGF19 on lipid metabolism in liver of large yellow croaker (Larimichthys crocea)","authors":"Jianlong Du ,&nbsp;Yuning Sun ,&nbsp;Jinze Zhang ,&nbsp;Wei Xu ,&nbsp;Kangsen Mai ,&nbsp;Qinghui Ai","doi":"10.1016/j.bbalip.2025.159700","DOIUrl":"10.1016/j.bbalip.2025.159700","url":null,"abstract":"<div><div>Fibroblast growth factor 19 (FGF19) is a key intestinally secreted factor in mammals, its physiological role in teleost remains largely unclear. This study aimed to investigate the function and underlying mechanisms of FGF19 in the regulation of lipid metabolism in large yellow croaker. Results revealed that FGF19 was predominantly expressed in the liver. Treatment with recombinant FGF19 protein significantly reduced triglyceride (TG) levels in hepatocytes in a dose-dependent manner. Both <em>in vitro</em> treatment and <em>in vivo</em> injection of FGF19 significantly downregulated lipogenic genes and upregulated lipolytic genes expression in hepatocytes and liver tissue. Further investigation demonstrated that FGFR1 inhibition attenuated the TG-lowering effects of FGF19 and reversed the suppression of lipogenic gene expression. Additionally, FGF19 treatment enhanced the phosphorylation of ERK, P38, AMPK, and AKT. Inhibition of P38, AMPK, or AKT significantly increased triglyceride levels which were reduced by FGF19. Inhibition of ERK, P38, and AKT impaired the FGF19-mediated regulation of lipolysis-related genes, whereas AMPK inhibition predominantly affected the regulation of lipogenic genes. Moreover, results showed that high linoleic acid (LA) intake induced endoplasmic reticulum stress and elevated expression of FGF19. The expression of XBP1s protein was significantly increased by LA treatment, while co-expression of XBP1s significantly induced the promoter activity of FGF19. In summary, these results suggest that FGF19 is primarily expressed in the liver and plays a crucial role in regulating lipid metabolism to prevent excessive lipid accumulation in large yellow croaker, while high LA intake can increase FGF19 expression through ER stress-induced XBP1s. This study will enhance the understanding of FGF19 in lipid metabolism, offering insights into the evolution of these processes in vertebrates.</div></div>","PeriodicalId":8815,"journal":{"name":"Biochimica et biophysica acta. Molecular and cell biology of lipids","volume":"1871 1","pages":"Article 159700"},"PeriodicalIF":3.3,"publicationDate":"2025-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145480691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}