Endocrine, metabolic & immune disorders drug targets最新文献

{"title":"The effects of Tissue-type Plasminogen Activator on PSC Activation.","authors":"Min Zha, Yi Wei, Shu Zhang","doi":"10.2174/0118715303394327251127145651","DOIUrl":"https://doi.org/10.2174/0118715303394327251127145651","url":null,"abstract":"<p><strong>Objective: </strong>Our previous studies have demonstrated that the activated pancreatic stellate cell (PSC) could induce islet damage in type 2 diabetes mellitus (T2DM). While tissue-type plasminogen activator (tPA) is significantly reduced in T2DM, its subsequent effects are unclear. The purpose of this experiment was to observe the impact of tPA on PSC activation, with the aim to better understand the potential role of tPA in T2DM.</p><p><strong>Methods: </strong>50 type 2 diabetic patients and 50 healthy persons were included in the diabetic group and the control group, respectively. Fasting blood was collected separately, and the tPA-level was detected by ELISA. Rat PSCs were isolated from pancreatic tissue using standard explant techniques. The PSCs were then characterized by staining them with Oil Red O to visualize lipid droplets and using immunofluorescent markers (α-smooth muscle actin (α-SMA), vimentin, and glial fibrillary acidic protein (GFAP)). After characterization, the PSCs were treated with tPA, then the proliferation of PSCs was measured using the cell counting kit-8 (CCK-8), the apoptosis was observed by the caspase-3 fluorometric assay kit, and the migration ability was assessed using the wound-healing assay and the transwell migration assay. Finally, a Western blot was used to identify the extracellular matrix (ECM) component synthesized by PSCs.</p><p><strong>Results: </strong>The diabetic patients had significantly lower levels of tPA compared to the controls. Rat PSCs treated with tPA exhibited more lipid droplet accumulation, and their ability of proliferation, migration, and ECM synthesis were significantly inhibited.</p><p><strong>Conclusion: </strong>This study demonstrated that tPA can play a crucial role in significantly inhibiting the activation, proliferation, migration, and ECM synthesis of PSC. Therefore, we speculate that the significant reduction of tPA in T2DM may exacerbate the detrimental effect of PSC on β-cell function.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Impact of Selenium Deficiency and Supplementation on Hashimoto's Thyroiditis: A Clinical Evaluation.","authors":"Hasan Acik, Yusuf Aydin","doi":"10.2174/0118715303424962251204064911","DOIUrl":"https://doi.org/10.2174/0118715303424962251204064911","url":null,"abstract":"<p><strong>Introduction: </strong>Hashimoto thyroiditis (HT) is an autoimmune disorder that leads to hypothyroidism. Selenium (Se) is essential for thyroid hormone metabolism and immune function, but its role in HT remains debated. This study investigates Se levels in HT patients and evaluates the impact of supplementation on thyroid autoimmunity and thyroid function.</p><p><strong>Methods: </strong>This retrospective study analyzed HT patients and healthy controls. Biochemical parameters, including Se, thyroid-stimulating hormone (TSH), free triiodothyronine (FT3), free thyroxine (FT4), anti-thyroid peroxidase (anti-TPO), and anti-thyroglobulin (anti-Tg) antibodies, were compared. Se-deficient HT patients (<80 µg/L) received selenium supplementation for six months. Paired t-tests and Spearman correlation analyses were used for statistical evaluation.</p><p><strong>Results: </strong>Among 270 HT patients and 350 controls, TSH levels were significantly elevated in HT (p<0.001), whereas Se levels showed no significant baseline difference (p=0.87). In Se-deficient patients (n=60), supplementation increased Se levels from 68.60±12.10 µg/L to 104.92±34.45 µg/L (p<0.001). However, anti-TPO and anti-Tg levels increased after treatment (p=0.01 and p=0.03, respectively). No significant changes were observed in TSH (p=0.27), FT3 (p=0.20), or FT4 (p=0.19). Se positively correlated with anti-TPO (r=0.36, p=0.0102) and negatively with FT3 (r=-0.39, p=0.0046).</p><p><strong>Discussion: </strong>Selenium supplementation restored serum Se levels but was unexpectedly associated with increased antibody titers. This finding contrasts with several randomized trials reporting antibody reduction, suggesting that baseline Se status, the form of supplementation, or differences in study design may account for the discrepancy. The observed correlations should be interpreted with caution.</p><p><strong>Conclusion: </strong>Selenium supplementation normalizes selenium status in HT patients, but its effects on thyroid autoimmunity and thyroid function remain uncertain. Long-term randomized controlled trials are needed to determine its therapeutic value.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research Hotspots and Emerging Frontiers in Ovarian Aging: A Bibliometric Analysis (2006-2025).","authors":"Qingquan Gong, Wenhong Ma, Chao Yang, Dingyu Liang, Yifu Wang, Yihua Yang, Mingyou Dong","doi":"10.2174/0118715303441084260119050045","DOIUrl":"https://doi.org/10.2174/0118715303441084260119050045","url":null,"abstract":"<p><strong>Introduction: </strong>Ovarian aging has a critical impact on women's fertility and overall health. This study uses bibliometric methods to analyze the current state of research in the field of natural ovarian aging and to identify emerging trends.</p><p><strong>Methods: </strong>This study analyzed 653 publications from the Web of Science Core Collection (2006-2025). Using VOSviewer and CiteSpace software, the authors visualized collaboration networks and identified research hotspots through co-occurrence and co-citation analyses.</p><p><strong>Results: </strong>Annual publications in the field of natural ovarian aging showed a significant upward trend; China and the United States were the main contributors to this research area. Huazhong University of Science and Technology and Nanjing Medical University were among the institutions with the highest number of publications. Wang SX was the author with the most publications, while Broekmans FJ was the most cited scholar. Human Reproduction was a core journal in this field. Keyword co-occurrence and reference co-citation analyses indicated that mitochondrial dysfunction, cellular senescence, inflammation, fibrosis, and multi-omics research were the research hotspots and frontiers during the study period.</p><p><strong>Discussion: </strong>The surge in keywords and citations suggests that the field is undergoing a fundamental shift from clinical phenotype studies to the exploration of molecular mechanisms. Findings in hotspot areas such as fibrosis and senescent cell clearance provide potential therapeutic targets for future clinical translation.</p><p><strong>Conclusion: </strong>This study employs bibliometric methods to map the current state of research, core themes, and emerging frontiers in the field of natural ovarian aging. The results offer researchers valuable insights into understanding the development trends in this field and guiding future research.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DHEAS Elevation as the Early Biochemical Abnormality in ACTH-Secreting Pituitary Microadenomas in Children: Two Case Reports.","authors":"Qiting Zhang, Yiling Cui, Wenjun Long, Ling Hou, Yanqin Ying, Xiaoping Luo","doi":"10.2174/0118715303421171260109070559","DOIUrl":"https://doi.org/10.2174/0118715303421171260109070559","url":null,"abstract":"<p><strong>Introduction: </strong>ACTH-secreting pituitary microadenomas are associated with insidious onset in children and atypical early clinical manifestations, making them highly susceptible to misdiagnosis and underdiagnosis. They are characterized by elevated ACTH and cortisol levels with a disrupted circadian rhythm. We reported two pediatric cases that showed significant elevation of Dehydroepiandrosterone Sulfate (DHEAS) and Androstenedione (Ad) in the early stage, while ACTH and cortisol were in the normal range or mildly abnormal.</p><p><strong>Case presentation: </strong>Case 1, a 13-year-old male, was admitted to the hospital with two years of growth retardation. The initial pituitary Magnetic Resonance Imaging (MRI) was normal. After one year, the patient developed Cushing's Syndrome (CS), and a repeat MRI suggested a pituitary microadenoma. Case 2, a 13.1-year-old female who had experienced excessive weight gain for two years and amenorrhea for 11 months. The child presented with CS initially, and the MRI revealed a pituitary microadenoma. Both of them were pathologically confirmed as ACTH-secreting pituitary microadenomas after Transsphenoidal Surgery (TSS).</p><p><strong>Conclusion: </strong>This report demonstrates that in cases with a significant DHEAS elevation, even with near-normal ACTH/cortisol levels and negative pituitary MRI, high clinical suspicion for ACTH- secreting microadenomas should be maintained, warranting close follow-up and further evaluation.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147848445","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated Bioinformatics Analysis of Autophagy-Related Biomarkers in Atherosclerosis and Acquired Immune Deficiency Syndrome.","authors":"Hua Zhong, Fangfang Zhang, Yupeng Wu, Yuzhu Zhang, Anxiang Sha, Zaihan Zhu, Min Bao, Dandan Sun","doi":"10.2174/0118715303453649260321063011","DOIUrl":"https://doi.org/10.2174/0118715303453649260321063011","url":null,"abstract":"<p><strong>Introduction: </strong>Atherosclerosis (AS) and acquired immune deficiency syndrome (AIDS) are associated with autophagy-related pathways. This research was intended to ascertain the interplay between AS and AIDS through autophagy-related mechanisms and to identify potential common biomarkers.</p><p><strong>Methods: </strong>Single-cell datasets for AS and AIDS were extracted from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) from each dataset were identified and then intersected with autophagy-related genes (ATGs). Functional enrichment and protein-protein interaction (PPI) network analyses were performed. Hub genes were determined via CytoHubba and MCODE. Finally, the hub genes were validated via bulk transcriptomic data. ROC curves were plotted, and their correlations with immune cell infiltration were investigated. Transcription factor networks and drug-gene interactions were implemented.</p><p><strong>Results: </strong>17 key ATGs were found, which were primarily enriched in autophagy, apoptosis, and TGF-β signaling pathways. After intersecting the 17 ATGs with DEGs using four algorithms in the Cytoscape plugin, eight genes were identified. Finally, three hub genes, encompassing GAPDH, HSPA8, and REL, were determined. ROC curves confirmed their diagnostic value. Their expression levels were markedly correlated with immune cell infiltration, and potential drugs were forecast.</p><p><strong>Discussion: </strong>This study demonstrates that GAPDH, HSPA8, and REL form a shared molecular pathway linking AS and AIDS via dysregulated autophagy, highlighting their potential as diagnostic biomarkers and therapeutic targets.</p><p><strong>Conclusion: </strong>Three hub genes, including GAPDH, HSPA8, and REL, were determined as potential biomarkers for AIDS and AS, providing insights into the molecular mechanisms of HIV-associated AS.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147793927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative eQTL and Mendelian Randomization Analyses with Experimental Validation Prioritize Genetic Candidate Biomarkers for Crohn's Disease.","authors":"Xinwei Zhang, Lin Liu, Wenyu Xu, Guangxin Li, Qiu Qin, Jinan Zhang","doi":"10.2174/0118715303433720260216212725","DOIUrl":"https://doi.org/10.2174/0118715303433720260216212725","url":null,"abstract":"<p><strong>Introduction: </strong>Crohn's disease (CD) is a chronic, idiopathic inflammatory bowel disease. Understanding the genetic and immunological basis of CD can lead to better therapeutic strategies.</p><p><strong>Methods: </strong>We employed publicly available datasets from the Gene Expression Omnibus (GEO) database to identify instrumental variables through expression quantitative trait loci (eQTL) analysis and conducted two-sample Mendelian randomization (MR) analyses. Additionally, we investigated the functions and pathways of co-expressed genes using GO, KEGG, and GSEA analyses. The association between these genes and immune cells was examined through immune cell infiltration assessment. Finally, the co-expressed genes were validated.</p><p><strong>Results: </strong>Several genes, including BATF2, SERPINB9, FCGR2A, MCTP1, SNX30, and SMIM1, were identified as having a causal relationship with CD. These genes are involved in important biological processes and pathways, including autoimmune regulation and oxidative stress. Moreover, CIBERSORT analysis demonstrated a unique distribution of immune cells in CD. Monocytes were significantly decreased in the disease group's tissues. Immune cell infiltration analysis further emphasized the distinct immune landscapes within this disease.</p><p><strong>Discussion: </strong>This study identified key genes associated with Crohn's disease, involving immune regulation and other factors, supplementing existing research. Despite limitations such as reliance on public data and insufficient experimental validation, the results provide a basis for exploring potential targets and conducting in-depth mechanism studies.</p><p><strong>Conclusion: </strong>The results of our study on the molecular mechanism of CD offer new insights into the identification of key genetic traits and potential therapeutic targets, which will enhance our understanding of the disease and lead to the development of more effective treatment options.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147793908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association Between Skeletal Muscle Mass to Visceral Fat Area Ratio and Hypertension: Mediation Analysis Involving Body Mass Index in the NHANES.","authors":"Juanjuan Fang, Zhenhua Wang, Apang Du, Yumin Ye, Jiangshui Yu, Yujing Huang, Markus W Ferrari","doi":"10.2174/0118715303444060260324064703","DOIUrl":"https://doi.org/10.2174/0118715303444060260324064703","url":null,"abstract":"<p><strong>Introduction: </strong>Body composition has emerged as a critical modulator of cardiovascular risk, and hypertension continues to be a significant public health concern. By combining harmful visceral fat with metabolically protective muscle, the skeletal muscle mass-to-visceral fat area ratio (SVR) may offer new insights into the pathophysiology of hypertension. The purpose of this study was to look into the mechanisms underlying the association between SVR and hypertension.</p><p><strong>Methods: </strong>Data from the National Health and Nutrition Examination Survey (2011-2018), which included 6,934 participants (27.2% of whom had hypertension), were analyzed in this cross-sectional study. The relationship between SVR and hypertension was investigated using Restricted Cubic Splines (RCS) and multivariable logistic regression. Mediation analysis was used to evaluate the impact of BMI. Gender, race, physical activity (Metabolic Equivalent of Task [MET] categories), metabolic comorbidities (diabetes, depression), smoking, and alcohol use were all subgroups analyzed.</p><p><strong>Results: </strong>Hypertensive individuals had significantly lower SVR (P < 0.001). After adjustments, a strong inverse association between SVR and hypertension was found. Individuals in the highest SVR quartile had 46% lower odds of hypertension (OR = 0.54, 95% CI: 0.36-0.82; P for trend < 0.004). RCS analysis revealed a nonlinear negative relationship between SVR and hypertension (P < 0.001) and a nonlinear positive association between BMI and hypertension (P < 0.001). Subgroup analyses indicated that the association persisted in metabolically healthy individuals (non-diabetic, non-depressed), Non-Hispanic White participants, moderate and heavy drinkers, and those with high MET levels (P < 0.05), but not in individuals with diabetes, depression, other racial/ethnic groups, light drinkers, or low-MET groups. Smoking significantly modified the relationship. BMI mediated 40.85% of the SVR-hypertension effect (P < 0.001).</p><p><strong>Discussion: </strong>This study is the first to explore the relationship between SVR and hypertension. A strong inverse correlation exists between SVR and the incidence of hypertension. The association between SVR and hypertension is stronger than that with BMI. A low SVR may amplify metabolic disorders through the synergistic effects of muscle mass and visceral fat. Although further experimental validation is still needed, these findings may provide new intervention strategies for the prevention of hypertension.</p><p><strong>Conclusion: </strong>Higher SVR is associated with a lower incidence of hypertension. As a composite measure of both skeletal muscle mass and visceral fat area, SVR provides more comprehensive insights into the link between body composition and high blood pressure.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147793949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rebound Thymic Hyperplasia after Recovery from Ectopic Cushing Syndrome: A Case Report and Literature Review.","authors":"Antonio Musolino, Elisa Cairoli, Alessandro Palleschi, Paola Toja, Manuela Chiodaroli, Sabrina Corbetta, Luca Persani, Valentina Morelli","doi":"10.2174/0118715303432270251209104836","DOIUrl":"https://doi.org/10.2174/0118715303432270251209104836","url":null,"abstract":"<p><strong>Introduction: </strong>Rebound thymic hyperplasia (RTH) is a rare benign condition resulting from compensatory proliferation of thymocytes after remission from stressful conditions, including hypercortisolism. Its appearance can sometimes be misleading, making differential diagnosis with thymic epithelial or neuroendocrine tumor challenging.</p><p><strong>Case presentation: </strong>We describe the case of a 31-year-old patient who was referred to our outpatient clinic for worsening hirsutism, acne, and fatigue. Biochemical and dynamic tests showed an ACTH-dependent hypercortisolism of ectopic origin (Ectopic Cushing syndrome, ECS). An enhanced total body CT scan was performed to localize the tumor, revealing a 14 mm peribronchial nodule in the left upper lung that was surgically removed, leading to hypercortisolism resolution and hypoadrenalism. During a follow-up chest-abdomen CT scan, an anterior mediastinal enlargement was found. To better characterize the lesion, the patient underwent an enhanced MRI, which provided a conclusive diagnosis of RTH. This allowed the medical team to avoid unnecessary and invasive surgical thymectomy.</p><p><strong>Conclusion: </strong>The present case highlights the diagnostic importance of recognizing RTH as a benign mimic of thymic tumors in adults recovering from ectopic Cushing syndrome. Misinterpretation may lead to unnecessary surgical intervention. MRI may be useful to characterize RTH in a non-invasive way. Successful treatment requires collaboration among endocrinologists, surgeons, and radiologists.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147793903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism of Gut Microbiota Dysbiosis in Insulin Resistance Polycystic Ovary Syndrome.","authors":"Fatimah Usman, Masagus Irsan Saleh, Kemas Yusuf Effendi, Peby Maulina Lestari, Widjiati Widjiati","doi":"10.2174/0118715303429583260303181915","DOIUrl":"https://doi.org/10.2174/0118715303429583260303181915","url":null,"abstract":"<p><strong>Introduction: </strong>Polycystic Ovary Syndrome (PCOS) is a complex endocrine disorder associated with insulin resistance, hyperandrogenism, and infertility. Gut microbiota dysbiosis is suspected to play a significant role in the pathogenesis of PCOS through the gut-brain-gonad axis, an axis that remains incompletely understood.</p><p><strong>Methods: </strong>This study aims to evaluate the role of gut microbiota dysbiosis in the mechanism of PCOS with insulin resistance by analyzing the abundance of <i>Lactobacillus sp.</i>, levels of Zonulin, Short Chain Fatty Acids (SCFAs), Insulin-Like Growth Factor-1 (IGF-1), and ovarian follicle count in a rat model of PCOS with insuline resistance, which in this study devided into 2 groups, control and treatment group, consist of 20 rats each. This experimental study employed an SEM-PLS approach to assess the relationships among microbiota, inflammation, metabolism, and ovarian function variables in an insulin-resistant PCOS rat model with insulin resistance.</p><p><strong>Results: </strong>The results showed decreases in Lactobacillus sp., SCFAs, and ovarian follicle counts, along with an increase in IGF-1 levels in PCOS model rats.</p><p><strong>Discussion: </strong>The study, utilizing an insulin-resistant Polycystic Ovary Syndrome (PCOS) rat model, established a strong, statistically significant link between gut microbiota dysbiosis and endocrine/ metabolic dysfunction. These were observed through increased levels of key markers: Zonulin (Control: 3.775, Treatment: 5.545), HOMA-IR (Control: 78.3400, Treatment: 140.9760), and IGF-1 (Control: 141.9665, Treatment: 189.5700). The Structural Equation Modeling (SEM) analysis confirmed two primary pathogenic pathways: (1) Gut Microbe/Metabolite Pathway: A reduction in beneficial <i>Lactobacillus sp.</i> was linked to lower SCFA levels, which influenced IGF-1 and negatively affected ovarian follicle development; (2) Inflammation/Insulin Resistance Pathway: The model established a statistically significant cascade where PCOS induction was strongly associated with Zonulin (β = -0.717), which then positively predicted HOMA-IR (β = 0.630), and HOMA-IR, in turn, strongly predicted IGF-1 (β = 0.662), defining the mechanism as PCOS → Zonulin → HOMA-IR → IGF-1.</p><p><strong>Conclusion: </strong>The dysbiosis mechanism involving gut microbiota in this study's model includes PCOS, Zonulin, HOMA-IR, and IGF-1, as these variables demonstrated statistically significant relationships.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147725282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Core Needle Biopsy (CNB) and Immunohistochemical Markers in Indeterminate Thyroid Nodules: Evidence and Perspectives.","authors":"Salvatore Monti, Valerio Renzelli, Beatrice Fazzalari, Claudia Bongermino, Maria Grazia Deiana, Giuseppe Pugliese","doi":"10.2174/0118715303433603251129105835","DOIUrl":"https://doi.org/10.2174/0118715303433603251129105835","url":null,"abstract":"<p><p>Thyroid nodules are a prevalent endocrine condition that requires accurate diagnostic tools to guide appropriate clinical management. Despite advances in imaging and cytology, evaluating thyroid nodules remains challenging, particularly in cases with indeterminate cytology. This narrative review examines the effectiveness of core needle biopsy (CNB) as a diagnostic approach, with a specific focus on its integration with immunohistochemical markers. CNB offers high diagnostic accuracy that improves with operator experience. The inclusion of immunohistochemical markers (CK19, CD56, Galectin-3, and HBME1) further enhances diagnostic precision, particularly in stratifying indeterminate nodules. However, CNB cannot reliably distinguish follicular adenoma from follicular carcinoma preoperatively because diagnosis requires evaluation of complete capsular and/or vascular invasion on the surgical specimen, which remains a fundamental limitation for follicular-patterned nodules. Despite its accuracy, broader adoption remains limited by non-standardized CNB protocols, inter-observer variability for IHC interpretation, and heterogeneous reimbursement policies across health systems, especially outside Western contexts. Comparative data on patient-reported outcomes and local cost-effectiveness in Asian and Indian settings are still variable and require multicenter validation before routine implementation can be generalized. The findings of this review reinforce the growing evidence that supports CNB as an effective diagnostic tool for thyroid nodules, especially when combined with immunohistochemical markers. This approach has the potential to improve diagnostic accuracy, reduce unnecessary surgical interventions, and enhance patient outcomes. Future research should focus on standardizing procedures and conducting large-scale validation studies.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147725312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}