Endocrine reviews最新文献

{"title":"Digestive Hormones and Their Impact on Bariatric and Pharmacologic Weight-Loss Therapies.","authors":"Maxime Amoyel, Claire Carette, Tigran Poghosyan, Johanne Le Beyec-Le Bihan, Maude Le Gall","doi":"10.1210/endrev/bnag032","DOIUrl":"https://doi.org/10.1210/endrev/bnag032","url":null,"abstract":"<p><p>Obesity is a growing global health challenge associated with major cardiometabolic complications. While bariatric surgery remains the most effective treatment for severe obesity, recent advances in incretin-based pharmacotherapy, multi-receptor agonists, and endoscopic bariatric procedures have substantially expanded therapeutic options. Beyond mechanical restriction, these interventions exert their effects through complex hormonal and neurophysiological mechanisms involving gut-brain signaling, gastric motility, and enteroendocrine adaptations. Gut-derived hormones, including ghrelin, glucagon-like peptide-1 (GLP-1), peptide YY (PYY), amylin, and leptin, play a central role in the regulation of hunger, satiation, and satiety by integrating nutrient sensing, vagal afferent signaling, and central hypothalamic pathways. Surgical procedures such as laparoscopic sleeve gastrectomy and Roux-en-Y gastric bypass induce profound and durable hormonal remodeling, whereas endoscopic sleeve gastroplasty primarily modulates gastric physiology with more modest and heterogeneous endocrine effects. Intragastric balloons induce a transient delay in gastric emptying and achieve moderate short-term weight loss, although their metabolic and weight-loss effects appear limited in durability. In parallel, GLP-1 receptor agonists and emerging multi-agonist therapies reproduce several post-bariatric hormonal adaptations and achieve clinically meaningful weight loss. In this review, we summarize current knowledge on digestive hormone physiology and provide an updated overview of the hormonal mechanisms underlying pharmacologic, endoscopic, and surgical bariatric interventions, highlighting their respective roles within a continuum of obesity treatment strategies.</p>","PeriodicalId":11544,"journal":{"name":"Endocrine reviews","volume":" ","pages":""},"PeriodicalIF":23.9,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711396","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":"Safeguarding the development of offspring: the role of genetic integrity of the maternal germline.","authors":"Xuebi Cai, Karla J Hutt, Amy L Winship, John Carroll, Andrew H Sinclair, Katie L Ayers, Elena J Tucker","doi":"10.1210/endrev/bnag027","DOIUrl":"https://doi.org/10.1210/endrev/bnag027","url":null,"abstract":"<p><p>Human development begins with the fusion of sperm and oocyte, yet the maternal genome plays a far more active and essential role than traditionally appreciated. This review critically examines the influence of maternal genetic integrity on embryogenesis and offspring health, emphasizing that the maternal genome is not merely a passive donor of half the DNA, but a vital architect of early life. We explore the role of maternal effect genes (MEGs) in orchestrating early zygotic development, detailing their functions in epigenetic regulation, mitochondrial dynamics, DNA repair, and cell division. A curated reference of MEGs, spanning mouse models and human pathogenic variants, is presented to support future research and clinical diagnostics. Beyond early embryonic development, maternal genetic integrity has lasting implications for offspring well-being. Errors in DNA replication and repair machinery within the maternal germline can lead to de novo variants (DNVs)-spontaneous germline variants that can be passed on to the offspring and impact their health at different ages. We highlight an underappreciated contribution of maternally derived DNVs to a growing list of sporadic disorders and present the first comprehensive catalogue of associated diseases. We further examine DNVs compatible with multigenerational transmission, investigating how maternal age and mutational processes-such as recombination errors and epigenetic drift-influence both disease risk and evolutionary outcomes. By integrating insights from developmental biology, genomics, and reproductive medicine, this review reframes the maternal genome as a dynamic and fragile foundation upon which life depends-offering new directions for understanding fertility, sporadic disease, and intergenerational health.</p>","PeriodicalId":11544,"journal":{"name":"Endocrine reviews","volume":" ","pages":""},"PeriodicalIF":23.9,"publicationDate":"2026-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148548333","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":"The metabolic roles of immune checkpoint molecules.","authors":"Yan Wang,Junxue Wang,Sijia Dan,Junke Zheng,Yingli Lu,Fangzhen Xia","doi":"10.1210/endrev/bnag030","DOIUrl":"https://doi.org/10.1210/endrev/bnag030","url":null,"abstract":"Immune checkpoint molecules (ICMs) are a class of surface proteins predominantly expressed on immune cells that play a key role in maintaining immune homeostasis by regulating the functions of T cells and other immune cells. Beyond their established immunoregulatory roles, emerging evidence indicates that ICMs are also involved in metabolic regulation. Within the tumor microenvironment (TME), tumour-derived ICMs have been shown to modulate glucose, amino acid, and lipid metabolism in infiltrating T cells, thereby influencing their metabolic reprogramming and functional states. Certain ICMs expressed on immune cells may directly regulate systemic metabolism through cell-intrinsic, immune-independent mechanisms. Moreover, specific ICMs are constitutively expressed in key metabolic tissues, such as pancreatic islets, liver, and adipose tissue, where they are thought to contribute to the maintenance of systemic metabolic homeostasis. Clinically, host metabolic status can affect the efficacy of immune checkpoint inhibitor (ICI) therapies. Conversely, ICI treatment can lead to metabolism-related adverse effects, such as ICI-associated diabetes (ICI-DM), which may extend beyond classic autoimmune insulin-dependent diabetes. Accumulating evidence suggests that ICMs can exert direct regulatory roles in metabolism independent of their canonical immune functions. Elucidating how ICMs regulate metabolism could, on the one hand, improve ICI therapy by maintaining metabolic homeostasis and preventing T cell exhaustion, and on the other hand, facilitate the development of novel therapeutic strategies for metabolic diseases that simultaneously target metabolic and inflammatory pathways. This review synthesises current knowledge on the metabolic roles and regulatory mechanisms of ICMs.","PeriodicalId":11544,"journal":{"name":"Endocrine reviews","volume":"22 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148522260","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":"Single-Cell Landscapes of Adipose-Derived Mesenchymal Stem Cells: From Homeostatic Regulators to Obesity-Driven Central Hubs.","authors":"Andreas Ritter,Nina-Naomi Kreis,Frank Louwen,Juping Yuan","doi":"10.1210/endrev/bnag029","DOIUrl":"https://doi.org/10.1210/endrev/bnag029","url":null,"abstract":"The prevalence of obesity is steadily increasing worldwide. Obesity profoundly alters the composition, structure, and function of adipose tissue (AT), the largest endocrine organ in the body. Adipose-derived mesenchymal stem cells (ASCs) are central to AT plasticity and become dysfunctional in obesity. In this review, we outline the molecular regulation of ASCs in self-renewal and differentiation, and their roles in regulating AT expansion, modulating immune and inflammatory response, and remodeling the extracellular matrix (ECM), positioning ASCs as decisive homeostatic regulators of AT. By integrating recent findings from cutting-edge studies and performing extensive bioinformatic analyses, we delineate ASC differentiation trajectories and propose a fundamentally revised view of ASCs with a heterogeneous hierarchy of functionally distinct subpopulations. Obesity impairs ASC subsets in their self-renewal and differentiation, driving fibro-inflammatory phenotypes that promote maladaptive immune response, ECM stiffening and fibrosis, and premature cellular senescence, acting as central hubs of obesity-associated tissue dysfunction. These alterations likely arise from reprogrammed ASC epigenomic landscapes and obesogenic niches characterized by an inflammatory milieu, toxic metabolites, and oxidative stress. Interestingly, substantial weight loss attenuates fibro-inflammatory stromal states and partially restores ASC pools, whereas fibrosis-associated transcriptional programs and niche memory persist, indicating incomplete reversal of obesity-induced stromal remodeling. Drawing on human, mouse, and experimental single-cell datasets, we provide mechanistic insights into the ASC-immune cell-ECM regulatory network, highlighting how obesity reshapes ASC identity, lineage trajectories, and niche signaling. Finally, we propose that therapeutic restoration of ASC plasticity may represent a promising strategy to reestablish AT homeostasis and limit the progression of metabolic disease.","PeriodicalId":11544,"journal":{"name":"Endocrine reviews","volume":"13 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148462230","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":"MASLD and the Cardiovascular-Kidney-Liver-Metabolic syndrome.","authors":"Angeliki M Angelidi, Chrysoula Boutari, Michail Kokkorakis, Konstantinos Stefanakis, Dimitri P Mikhailidis, George Jacob, Christos S Mantzoros","doi":"10.1210/endrev/bnag023","DOIUrl":"https://doi.org/10.1210/endrev/bnag023","url":null,"abstract":"<p><p>Obesity is an alarmingly growing global epidemic strongly associated with type 2 diabetes, cardiovascular disease, metabolic syndrome, and chronic kidney disease. Metabolic dysfunction-associated steatotic liver disease (MASLD) is considered an important contributor within this interconnected spectrum, representing a new component of the broader cardio-kidney-metabolic (CKM) syndrome, now more aptly labelled as the cardio-kidney-liver-metabolic (CKLM) syndrome. This narrative review synthesizes evidence from epidemiological studies, clinical trials, and ongoing scientific research to explore the multifaceted associations, complex interplay and shared pathophysiological mechanisms among these disorders. The clinical implications of this interplay are substantial, underscoring the need for a holistic approach encompassing early detection, comprehensive risk assessment, and multi-targeted interventions. Therapeutic strategies discussed include lifestyle modification, anti-diabetic, anti-obesity, lipid-lowering agents, and bariatric surgery. Given MASLD's potential role in the CKLM spectrum, future research should deepen the understanding of shared mechanisms and develop integrated clinical management strategies to improve outcomes and reduce their global burden.</p>","PeriodicalId":11544,"journal":{"name":"Endocrine reviews","volume":" ","pages":""},"PeriodicalIF":23.9,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148445051","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":"Epigenetics and disease progression in neuroendocrine neoplasms.","authors":"Eduardo C Lobato, Andre F Lafranchi, Felipe Freitas-Castro, Gustavo F C Fagundes, Bekim Sadikovic, Kate E Lines, Madson Q Almeida","doi":"10.1210/endrev/bnag005","DOIUrl":"10.1210/endrev/bnag005","url":null,"abstract":"<p><p>Epigenetic regulation, including DNA methylation, histone modifications, non-coding RNAs, and higher-order chromatin remodeling, plays a central role in the biology of neuroendocrine neoplasms (NENs). Advances in high-throughput profiling have uncovered epigenetic alterations across pheochromocytomas/paragangliomas (PPGLs), gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs), lung neuroendocrine neoplasms (LNENs), medullary thyroid carcinoma (MTC), and pituitary NETs (PitNETs). These alterations converge on pathways governing cell cycle control, telomere maintenance, hypoxia signaling, epithelial-mesenchymal transition, and chromatin architecture. Importantly, epigenetic signatures not only mirror genetic backgrounds (eg, SDHx, MEN1, ATRX, RET) but also provide independent layers of prognostic and predictive information. Distinct methylation profiles, histone modification patterns, and deregulated microRNA/long non-coding RNA networks have been consistently linked to tumor aggressiveness, metastatic potential, and therapeutic resistance. The clinical translation of these insights is rapidly evolving. Methylation-based classifiers and circulating epigenetic markers are emerging as promising tools for early diagnosis, risk stratification, and longitudinal monitoring. Moreover, epigenetic pathways represent attractive therapeutic targets, with DNA methyltransferase inhibitors, histone deacetylase inhibitors, and RNA-modifying enzyme modulators under active investigation. However, significant challenges remain, including methodological heterogeneity, small or retrospective cohorts, and the limited functional validation of candidate biomarkers. Future priorities include prospective multi-institutional validation, integration of epigenomics with other molecular layers in multidimensional classifiers, and the application of spatial and single cell approaches to resolve intra-tumoral heterogeneity. Ultimately, epigenetic research has redefined our understanding of NEN pathogenesis and progression, positioning the epigenome as a promising frontier in precision oncology. Through robust validation, epigenetic biomarkers and therapies may transform the clinical management of NENs.</p>","PeriodicalId":11544,"journal":{"name":"Endocrine reviews","volume":" ","pages":"422-467"},"PeriodicalIF":23.9,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146200406","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":"Steroid receptor coactivators: from basic research to translational opportunities.","authors":"Yosef Gilad, Sang Jun Han, David M Lonard","doi":"10.1210/endrev/bnag003","DOIUrl":"10.1210/endrev/bnag003","url":null,"abstract":"<p><p>The concept of nuclear receptor (NR) coregulation was proposed nearly 2 decades before it was experimentally validated. According to this model, NRs-executors of a vast array of transcriptional programs-do not act independently but are governed by a network of regulatory proteins that either activate or repress their biological function. Nuclear receptors identify the genes to be regulated. However, coregulators ultimately serve as the true controllers of transcriptional outcomes. They recruit cofactors and coordinate the activity of transcriptional complexes, thereby shaping NR-mediated gene expression beyond NRs' intrinsic functionality. The steroid receptor coactivator (SRC) family is the most extensively studied and functionally dominant group of NR coregulators, modulating nearly all gene activities. The pleiotropic biological roles of SRCs-spanning key physiological and pathological processes-make them compelling therapeutic targets. Here, we outline the evolution of the coregulation concept, which reached a critical milestone with the discovery of the SRC family. We highlight the central roles of SRCs in both physiology and oncology and trace the development of therapeutic strategies aimed at targeting these proteins.</p>","PeriodicalId":11544,"journal":{"name":"Endocrine reviews","volume":" ","pages":"399-421"},"PeriodicalIF":23.9,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13368381/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146257812","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":"Genetic and environmental drivers of craniofacial, brain, and pituitary disorders.","authors":"Sally A Camper,Julian Martinez-Mayer,Shalini Guha,Nooshin Mojahed,Leonard Y M Cheung,Stefan H Geyer,Michelle L Brinkmeier,Wolfgang J Weninger,Hironori Bando,Lori T Raetzman,María I Pérez Millán,Buffy S Ellsworth,Marika Charalambous,Shannon W Davis","doi":"10.1210/endrev/bnag028","DOIUrl":"https://doi.org/10.1210/endrev/bnag028","url":null,"abstract":"Congenital pituitary hormone deficiency (CH) is a rare disorder that usually involves deficient production of growth hormone (GH) and other pituitary hormones. Many cases are syndromic, affecting other aspects of craniofacial development and sometimes other organs. There are many genes implicated in congenital pituitary hormone deficiency, and some of them also cause more severe disorders like septo-optic dysplasia (SOD) and holoprosencephaly (HPE). It is not clear why mutations in the same gene can cause such variable clinical features. In addition, the molecular etiology of many cases is not identified with current genetic testing approaches. To realize the promise of the human genome project, more genetic causes need to be identified, and the basis for variable clinical presentations needs to be better understood. In this review we provide information about the overlapping genetic causes of this spectrum of disorders in humans, discuss the influence of genetic background and environment on presentations, and highlight animal models that expand our understanding of how genetic and environmental factors can synergize to generate diverse phenotypes. Evidence for genetic and environmental contributions to this spectrum of disorders is strong.","PeriodicalId":11544,"journal":{"name":"Endocrine reviews","volume":"6 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148441293","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":"Management of postmenopausal osteoporosis.","authors":"Ian R Reid, Mark J Bolland","doi":"10.1210/endrev/bnag006","DOIUrl":"10.1210/endrev/bnag006","url":null,"abstract":"<p><p>Postmenopausal women experience ongoing loss of bone mass, with resulting increases in the risk of fracture. This review describes the nature of postmenopausal bone loss, the definition of osteoporosis, and the current status of fracture risk estimation, which is pivotal in osteoporosis management. Important lifestyle measures include taking a balanced diet to maintain a healthy weight throughout life, safe physical activity, not smoking, and moderating alcohol intake. Severe vitamin D deficiency accelerates bone loss so should be avoided. Falls prevention becomes increasingly important with age, since falls cause most fractures. Pharmaceuticals to increase bone mass and prevent fractures either act by inhibiting bone resorption or by stimulating bone formation. Bisphosphonates are the most widely used antiresorptives, often taken as weekly oral doses. The intravenous bisphosphonate, zoledronate, has a long duration of action with effects on bone turnover, density, and fractures over a decade after a single dose. It is increasingly used in both prevention and treatment of osteoporosis. Denosumab is effective in preventing fractures but has a rapid offset of effect after its cessation. Some anabolic agents act via the PTH1 receptor, producing substantial increases in spine bone density but are not yet proven to prevent hip fractures. Romosozumab is a monoclonal antibody directed at sclerostin. It has both anabolic and antiresorptive effects and shows broad antifracture efficacy. Anabolics are used for 1 to 2 years in those with high fracture risk, before transition to long-term antiresorptive therapy. Treatment sequence options are discussed but more research is needed to establish which provide optimal fracture reduction.</p>","PeriodicalId":11544,"journal":{"name":"Endocrine reviews","volume":" ","pages":"468-495"},"PeriodicalIF":23.9,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13368380/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147303596","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":"Stanniocalcin 1 at the nexus of calcium homeostasis, IGF signaling, and cancer immunity.","authors":"Cunming Duan","doi":"10.1210/endrev/bnag026","DOIUrl":"https://doi.org/10.1210/endrev/bnag026","url":null,"abstract":"The textbook view of the regulation of calcium homeostasis centers on parathyroid hormone, calcitriol, and calcitonin. While this paradigm has long dominated the field, it represents only part of a broader evolutionary and physiological landscape. This article focuses on Stanniocalcin 1 (STC1), a calciotropic hormone originally discovered in bony fish. Since its discovery in the 1970s, our understanding of STC1 has evolved from a \"fish-specific\" hormone to a member of a multifunctional glycoprotein family with deep roots in metazoan evolution. Recent studies in zebrafish show that STC1 inhibits calcium uptake through two mechanisms: it reduces TRPV6-dependent calcium influx and limits the proliferation of calcium-transporting ionocytes. Mechanistically, STC1 suppresses local insulin-like growth factor (IGF) signaling by binding pappalysin-family IGF-binding protein (IGFBP) proteases, thereby modulating IGFBP processing and downstream IGF activity. This STC1-Pappalysin-IGFBP-IGF axis has recently been positioned as a central node in an organ-brain communication pathway that links calcium uptake to brain function and animal behavior. In humans and other mammals, STC1 is expressed in many tissues locally and exerts local actions in a paracrine fashion. Dysregulation of STC1 expression has been associated with chronic kidney diseases and multiple cancer types. Recent studies have uncovered a novel role for STC1 in tumor immune evasion as a phagocytosis checkpoint and a \"don't eat me\" signal. This review integrates recent findings on the multifunctional roles of STC1 in regulating calcium homeostasis, IGF signaling, and cancer immunity, and to highlight the therapeutic potential of targeting STC1 in kidney diseases and cancer immunotherapy.","PeriodicalId":11544,"journal":{"name":"Endocrine reviews","volume":"18 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148432594","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}