Journal of molecular endocrinology最新文献

Mechanistic insights of Rhodiola crenulata in treating diabetic kidney disease via network pharmacology. 红景天治疗糖尿病肾病的网络药理学机制探讨。

IF 3.6 4区医学

Journal of molecular endocrinology Pub Date : 2025-06-01 DOI: 10.1530/JME-25-0006

Junhan Li, Yuying Cui, Jinming Yao, Congcong Guo, Mingwen Jiao

{"title":"Mechanistic insights of Rhodiola crenulata in treating diabetic kidney disease via network pharmacology.","authors":"Junhan Li, Yuying Cui, Jinming Yao, Congcong Guo, Mingwen Jiao","doi":"10.1530/JME-25-0006","DOIUrl":"https://doi.org/10.1530/JME-25-0006","url":null,"abstract":"Rhodiola crenulata (RC) has long been used in traditional medicine for its health benefits, including managing high-altitude sickness, fatigue, and diabetes. Diabetic kidney disease (DKD) is a severe diabetes consequence, often leading to progressive renal fibrosis. This study investigated how RC helps protect against kidney fibrosis in DKD rat models, focusing on identifying active compounds and their therapeutic targets, especially the effects of salidroside (SAL), a key component of RC. After administering RC to DKD rats, 22 core components were identified and analyzed via network pharmacology, leading to 141 DKD-related therapeutic targets. The compound SAL showed significant targeting capability, implicating TGFB1 as a primary therapeutic target in kidney fibrosis. In vivo, the study assessed RC's effects on fibrosis markers, while in vitro analyses explored SAL's role in fibroblast activation and TGF-β1 regulation in proximal renal tubular epithelial cells (PTECs). We found that RC treatment effectively reduced fibrosis markers in DKD rats by decreasing glomerular mesangial expansion, collagen deposition, and myofibroblast proliferation, alongside decreasing TGF-β1 levels. In vitro, SAL inhibited high glucose-induced fibroblast activation and TGF-β1 expression in PTECs, suggesting its direct role in slowing fibrosis progression. We conclude that the antifibrotic effects of RC in DKD may be attributed to SAL's ability to regulate fibroblast activity and suppress TGF-β1. These findings highlight its potential as a therapeutic component for DKD management.","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144285032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effect of metformin on the endometrial proteome of diet-induced obese mice. 二甲双胍对饮食性肥胖小鼠子宫内膜蛋白质组的影响。

IF 3.6 4区医学

Journal of molecular endocrinology Pub Date : 2025-04-24 Print Date: 2025-05-01 DOI: 10.1530/JME-24-0098

Maria-Nefeli Malliou-Becher, Eva-Maria Turnwald, Lara Skupin, Tobias Kretschmer, Andrea Mesaros, Martin Purrio, Maria Wohlfarth, Marion Handwerk, Simone Kalis, Dirk Gründemann, Jörg Dötsch, Ariane Germeyer, Sarah Appel

{"title":"Effect of metformin on the endometrial proteome of diet-induced obese mice.","authors":"Maria-Nefeli Malliou-Becher, Eva-Maria Turnwald, Lara Skupin, Tobias Kretschmer, Andrea Mesaros, Martin Purrio, Maria Wohlfarth, Marion Handwerk, Simone Kalis, Dirk Gründemann, Jörg Dötsch, Ariane Germeyer, Sarah Appel","doi":"10.1530/JME-24-0098","DOIUrl":"https://doi.org/10.1530/JME-24-0098","url":null,"abstract":"Obesity is known to have detrimental effects on female fertility, influencing both ovarian and endometrial functions. There is evidence that endometrial function is altered in obese and/or insulin-resistant women. Metformin, an insulin-sensitizing drug, has shown potential in treating metabolic and reproductive disorders, including polycystic ovary syndrome (PCOS) and may enhance fertility outcomes by improving endometrial dysfunction. Using a mouse model, this study aimed to investigate how a high-fat diet impacts endometrial-specific protein expression and whether metformin can mitigate these effects. C57BL/6N mice were fed a standard or high-fat diet and either received metformin treatment or did not. Proteomic analyses revealed significant alterations in endometrial protein expression due to the high-fat diet, while metformin administration appeared to restore many of these changes to normal levels. Metformin's impact was evident through alterations in specific proteins associated with reproductive health and metabolic functions, such calcium-independent phospholipase A2-gamma, ATP-binding cassette sub-family D member 1, RAC-beta serine/threonine-protein kinase, acyl-CoA:lysophosphatidylglycerol acyltransferase 1, O-GlcNAcase, scavenger receptor class A member 3, protein kinase C beta type, sortilin, beta-2-microglobulin and apolipoprotein C-III. These results suggest a potential therapeutic role for metformin in normalizing endometrial protein expression, providing insights into how this drug could improve fertility outcomes in obese or insulin-resistant females, besides normalizing ovulation patterns. Overall, this study enhances our understanding of the relationship among obesity, endometrial function and metformin's therapeutic potential, offering a foundation for further research into reproductive health and metabolic disorders.","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":"74 4","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144014944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Identification of anti-resorptive GPCRs by high-content imaging in human osteoclasts. 利用高含量显像技术鉴定人破骨细胞的抗再吸收gpcr。

IF 3.6 4区医学

Journal of molecular endocrinology Pub Date : 2025-04-22 Print Date: 2025-05-01 DOI: 10.1530/JME-24-0143

Maria L Price, Rachael A Wyatt, Joao Correia, Zakia Areej, Maisie Hinds, Ana Crastin, Rowan S Hardy, Morten Frost, Caroline M Gorvin

{"title":"Identification of anti-resorptive GPCRs by high-content imaging in human osteoclasts.","authors":"Maria L Price, Rachael A Wyatt, Joao Correia, Zakia Areej, Maisie Hinds, Ana Crastin, Rowan S Hardy, Morten Frost, Caroline M Gorvin","doi":"10.1530/JME-24-0143","DOIUrl":"https://doi.org/10.1530/JME-24-0143","url":null,"abstract":"Osteoporosis diagnoses are increasing in the ageing population, and although some treatments exist, these have several disadvantages, highlighting the need to identify new drug targets. G protein-coupled receptors (GPCRs) are transmembrane proteins whose surface expression and extracellular activation make them desirable drug targets. Our previous studies have identified 144 GPCR genes to be expressed in primary human osteoclasts, which could provide novel drug targets. The development of high-throughput assays to assess osteoclast activity would improve the efficiency at which we could assess the effect of GPCR activation on human bone cells and could be utilised for future compound screening. Here, we assessed the utility of a high-content imaging (HCI) assay that measured cytoplasmic-to-nuclear translocation of the nuclear factor of activated T cells-1 (NFATc1), a transcription factor that is essential for osteoclast differentiation, and resorptive activity. We first demonstrated that the HCI assay detected changes in NFATc1 nuclear translocation in human primary osteoclasts using GIPR as a positive control, and then developed an automated analysis platform to assess NFATc1 in nuclei in an efficient and unbiased manner. We assessed six GPCRs simultaneously and identified four receptors (FFAR2, FFAR4, FPR1 and GPR35) that reduced osteoclast activity. Bone resorption assays and measurements of TRAP activity verified that activation of these GPCRs reduced osteoclast activity, and that receptor-specific antagonists prevented these effects. These studies demonstrate that HCI of NFATc1 can accurately assess osteoclast activity in human cells, reducing observer bias and increasing efficiency of target detection for future osteoclast-targeted osteoporosis therapies.","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":"74 4","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12023344/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143997181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lack of maternal exposure to somatostatin leads to diet-induced insulin and leptin resistance in mouse male offspring. 缺乏母体生长抑素暴露导致小鼠雄性后代饮食诱导的胰岛素和瘦素抵抗。

IF 3.6 4区医学

Journal of molecular endocrinology Pub Date : 2025-03-22 Print Date: 2025-05-01 DOI: 10.1530/JME-24-0102

Zhongyue Yang, Catherine P Kirschke, Liping Huang

{"title":"Lack of maternal exposure to somatostatin leads to diet-induced insulin and leptin resistance in mouse male offspring.","authors":"Zhongyue Yang, Catherine P Kirschke, Liping Huang","doi":"10.1530/JME-24-0102","DOIUrl":"10.1530/JME-24-0102","url":null,"abstract":"Somatostatin (Sst) is an inhibitory regulator of many hormones. The prenatal environment impacts an offspring's risk to type 2 diabetes in adulthood. However, the effect of maternal Sst deficiency on glucose and insulin metabolism in offspring and metabolic disease risk in their adult life has been poorly understood. The study was to investigate the impact of a lack of maternal Sst exposure in mouse male and female offspring on diet-induced changes in glucose metabolism and adiposity. Sst knockout offspring, SstKO born to the Sst-heterozygous dams or SstKO-MSD born to the Sst-homozygous dams were fed either a regular diet (CD) or a high-fat diet (HFD) at 3-week-old for 15 weeks. Body weight and blood glucose levels were monitored. Glucose and insulin tolerance tests were performed. Plasma hormone levels and gene expression in the hypothalamus were investigated. The results demonstrated that only male SstKO-MSD offspring developed obesity accompanied by severe insulin and leptin resistance after HFD challenge. Insulin secretion was reduced in both basal and oral glucose-challenged conditions in the CD-fed male SstKO-MSD mice. A reduced ratio of islet area to pancreas area was noted in SstKO-MSD mice in both sexes. Plasma levels of glucagon, Glp1 and Pyy were elevated in both male and female SstKO and SstKO-MSD mice. mRNA expression of leptin receptor, FoxO1, Npy and Agrp was downregulated in male SstKO-MSD mice. These results demonstrate that a lack of fetal somatostatin exposure impairs the islet development in offspring and increases risk of obesity, insulin resistance and leptin resistance later in life.","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11964479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Disruption of thyroid-intrinsic clock aggravates experimental autoimmune thyroiditis. 甲状腺内在时钟紊乱加重实验性自身免疫性甲状腺炎。

IF 3.6 4区医学

Journal of molecular endocrinology Pub Date : 2025-03-08 Print Date: 2025-04-01 DOI: 10.1530/JME-25-0022

Jinrong Fu, Rili Gao, Qiting Ye, Wenwen Feng, He Liu, Yushu Li, Haixia Guan

引用次数: 0

Anti-inflammatory effects of palm11-PrRP31 in a rat model of lipopolysaccharide-induced acute inflammation. 棕榈11-PrRP31在脂多糖诱发急性炎症大鼠模型中的抗炎作用

IF 3.6 4区医学

Journal of molecular endocrinology Pub Date : 2025-02-14 Print Date: 2025-04-01 DOI: 10.1530/JME-24-0090

Lucia Mráziková, Silvie Hojná, Anna Shánělová, Blanka Železná, Jaroslav Kuneš, Lenka Maletínská

{"title":"Anti-inflammatory effects of palm11-PrRP31 in a rat model of lipopolysaccharide-induced acute inflammation.","authors":"Lucia Mráziková, Silvie Hojná, Anna Shánělová, Blanka Železná, Jaroslav Kuneš, Lenka Maletínská","doi":"10.1530/JME-24-0090","DOIUrl":"10.1530/JME-24-0090","url":null,"abstract":"Lipopolysaccharides (LPS) are major components of gram-negative bacteria. LPS not only induce endotoxemia and inflammation but also contribute to various diseases. In experimental settings, LPS administration serves as a model for acute inflammatory responses. This study aimed to evaluate the anti-inflammatory potential and mechanism of action of palmitoylated prolactin-releasing peptide (palm11-PrRP31) in a rat model of LPS-induced inflammation. Palm11-PrRP31 has demonstrated efficacy in mitigating LPS-induced weight loss and anorexia, emphasizing its potential protective effects. The cytokine profiles revealed a consistent reduction in tumor necrosis factor α, highlighting the potent anti-inflammatory effects of palm11-PrRP31. The peptide also modulated key cytokines and chemokines in the plasma, liver and hypothalamus, reflecting its broad-spectrum anti-inflammatory properties. Palm11-PrRP31 also effectively attenuated the expression levels of Toll-like receptor 4 signaling components in the liver, suggesting its ability to suppress the activation of these pathways during LPS-induced inflammation. These anti-inflammatory effects were specific to palm11-PrRP31, whereas natural PrRP31 had a minimal impact. In conclusion, this study reveals the efficacy of palm11-PrRP31 in modulating LPS-induced inflammation, offering insights into its immunomodulatory properties. The ability of the peptide to suppress proinflammatory responses and attenuate relevant signaling pathways indicates its potential use as a therapeutic agent for inflammatory disorders.","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11840832/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143052745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dicer inhibition delays wound closure by increasing Suz12 levels and regulating ITGAV levels in keratinocytes. Dicer抑制通过增加角化细胞中SUZ12水平和调节ITGAV水平来延迟伤口愈合。

IF 3.6 4区医学

Journal of molecular endocrinology Pub Date : 2025-01-28 Print Date: 2025-03-01 DOI: 10.1530/JME-24-0122

Sushant Bhattacharya, Shruti Hazra, Malabika Datta

{"title":"Dicer inhibition delays wound closure by increasing Suz12 levels and regulating ITGAV levels in keratinocytes.","authors":"Sushant Bhattacharya, Shruti Hazra, Malabika Datta","doi":"10.1530/JME-24-0122","DOIUrl":"10.1530/JME-24-0122","url":null,"abstract":"Delayed wound closure is a significant hallmark associated with diabetes. A previous study from our laboratory identified decreased levels of Dicer and miRNAs together with altered levels of wound-healing genes in the wounded tissues of diabetic rats. Comprehensive regulators of these wound-healing genes mapped onto the PRC2 (polycomb repressive complex 2) complex. Here, we show that Dicer inhibition increases the transcript levels of core components of the PRC2 complex, namely Suz12 (suppressor of zeste 12) and Ezh2 (enhancer of zeste 2), and of Mtf2 (metal response element-binding transcription factor 2), its additional subunit, and elevates H3K27me3 levels in HaCaT cells. Such patterns of increase were also observed in the wounded tissues of diabetic rats as compared to those of normal rats. In a scratch assay in HaCaT cells, while Dicer inhibition significantly prevented wound closure, this was rescued by Suz12 siRNA but not by Ezh2 inhibition, suggesting that Suz12 mediates the effects of Dicer siRNA in these cells. In addition, as compared to scramble-transfected cells, Dicer siRNA decreased the levels of integrin alpha V (Itgav), which is extensively implicated in the process of wound healing, and this effect was rescued in the presence of Suz12 siRNA. Itgav harbours potential histone methylation marks across the gene length, and Dicer inhibition, by increasing PRC2-mediated H3K27 methylation on Itgav, possibly decreases its transcription that subsequently impairs wound closure. These data put forth novel aspects of delayed wound closure as seen during diabetes and might be a potential target for therapeutic intervention.","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142978975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A missing paradigm: deciphering endocrine innovations among diverging regulations of alleles, paralogous genes and orthologous genes. 一个缺失的范例：在等位基因、旁系和同源基因的不同调控中破译内分泌创新。

IF 3.6 4区医学

Journal of molecular endocrinology Pub Date : 2025-01-11 Print Date: 2025-02-01 DOI: 10.1530/JME-24-0092

Jean-Jacques Lareyre, Philippe Monget

引用次数: 0

Glucocorticoids reduce Slc2a2 (GLUT2) gene expression through HNF1 in pancreatic β-cells. 糖皮质激素通过HNF1降低胰腺β-细胞中Slc2a2 （GLUT2）基因的表达。

IF 3.6 4区医学

Journal of molecular endocrinology Pub Date : 2025-01-10 Print Date: 2025-02-01 DOI: 10.1530/JME-24-0077

Yuka Ono, Kohsuke Kataoka

{"title":"Glucocorticoids reduce Slc2a2 (GLUT2) gene expression through HNF1 in pancreatic β-cells.","authors":"Yuka Ono, Kohsuke Kataoka","doi":"10.1530/JME-24-0077","DOIUrl":"10.1530/JME-24-0077","url":null,"abstract":"Glucose transporter type 2 (GLUT2), encoded by the Slc2a2 gene, is essential for glucose-stimulated insulin secretion (GSIS) in pancreatic islet β-cells, and low expression of GLUT2 is associated with β-cell dysfunction during the progression of type 2 diabetes in humans and animal models. Glucocorticoids are stress hormones that regulate inflammation and metabolism through the glucocorticoid receptor (GR), a member of the nuclear receptor superfamily, and synthetic glucocorticoids are widely used for the treatment of inflammatory disorders. Prolonged exposure to glucocorticoids induces β-cell dysfunction and diabetes, but the effects of Slc2a2 gene repression in β-cells, if any, and the mechanisms involved remain unclear. In the present study, we measured the expression of GSIS-related genes in the MIN6 β-cell line and found that Slc2a2 mRNA expression was selectively reduced by dexamethasone (DEX), a synthetic glucocorticoid. Using bioinformatics and reporter assays, we identified two β-cell enhancers of the Slc2a2 gene, one within the first intron and another located approximately 40 kb downstream of the transcription start site. The latter enhancer (designated as E3c) was responsible for the DEX-induced repression of the Slc2a2 gene. Of the previously identified β-cell-enriched transcription factors (NEUROD1, MAFA, HNF1α and HNF1β) that activate the E3c enhancer, the transcriptional activity of HNF1α and HNF1β, responsible for maturity-onset diabetes of the young types 3 and 5, respectively, was repressed by DEX and GR. This functional link between HNF1α/HNF1β and GR should help elucidate the mechanism of glucocorticoid-induced β-cell dysfunction and diabetes.","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142837163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of mu-opioid receptors in pancreatic islet α-cells. 胰岛α细胞中缪阿片受体的作用

IF 3.6 4区医学

Journal of molecular endocrinology Pub Date : 2024-12-20 Print Date: 2025-01-01 DOI: 10.1530/JME-24-0060

Chen Kong, Daniel C Castro, Jeongmin Lee, David W Piston

{"title":"The role of mu-opioid receptors in pancreatic islet α-cells.","authors":"Chen Kong, Daniel C Castro, Jeongmin Lee, David W Piston","doi":"10.1530/JME-24-0060","DOIUrl":"10.1530/JME-24-0060","url":null,"abstract":"Diabetes is a complex disease that impacts more than 500 million people across the world. Many of these individuals will develop diabetic neuropathy as a comorbidity, which is historically treated with exogenous opioids, such as morphine, oxycodone, or tramadol. Although these opioids are effective analgesics, growing evidence indicates that they may directly impact the endocrine pancreas function in patients. One common feature of these exogenous opioid ligands is their preference for the mu-opioid receptor (MOPR), so we aimed to determine whether endogenous MOPRs directly regulate pancreatic islet metabolism and hormone secretion. We show that pharmacological antagonism of MOPRs enhances glucagon secretion, but not insulin secretion, from human islets under high-glucose conditions. This increased secretion is accompanied by increased cAMP signaling. mRNA expression of MOPRs is robust in nondiabetic human islets but downregulated in islets from T2D donors, suggesting a link between metabolism and MOPR expression. Conditional genetic knockout of MOPRs in murine α-cells increases glucagon secretion under high-glucose conditions without increasing glucagon content. Consistent with downregulation of MOPRs during metabolic disease, conditional MOPR knockout mice treated with a high-fat diet show impaired glucose tolerance, increased glucagon secretion, increased insulin content, and increased islet size. Together, these results demonstrate a direct mechanism of action for endogenous opioid regulation of endocrine pancreas.","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.6,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11875080/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142546030","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0