Endocrine, metabolic & immune disorders drug targets最新文献

{"title":"Paricalcitol Attenuates Bleomycin-induced Pulmonary Fibrosis: Insights from Immunohistochemical and Molecular Genetic Analysis.","authors":"Maxim A Kriventsov, Darya A Enzel, Tatyana P Sataieva","doi":"10.2174/0118715303434362251212040431","DOIUrl":"10.2174/0118715303434362251212040431","url":null,"abstract":"<p><strong>Introduction: </strong>Pulmonary fibrosis is a progressive disease marked by excessive fibrotic transformation of lung tissue. Paricalcitol, a selective vitamin D receptor (VDR) agonist, has shown promise in reducing fibrosis in experimental models, primarily due to its anti-inflammatory and anti-fibrotic properties. This study evaluates the therapeutic effects of paricalcitol on bleomycin-induced pulmonary fibrosis in a rat model.</p><p><strong>Materials and methods: </strong>Fifty-four male Wistar rats were randomly assigned to three groups: a control group, a bleomycin-induced pulmonary fibrosis group (PF), and a bleomycin-induced pulmonary fibrosis group with paricalcitol treatment (PF+P). Pulmonary fibrosis was induced via intratracheal bleomycin instillation, and paricalcitol was administered every two days to the PF+P group. Effects were assessed through histopathological, immunohistochemical, and molecular genetic analyses, including mRNA expression levels of inflammatory and fibrotic markers at 10, 20, and 30 days.</p><p><strong>Results: </strong>Paricalcitol treatment significantly reduced fibrosis severity, with the Aschoff score decreasing on day 30 to 2.50±0.63 compared with 5.88±0.52 in untreated PF rats (p = 0.02). The number of CD80+ M1 macrophages was reduced on day 10 (29.9±3.8 vs 64.2±5.2, p = 0.001), while CD163+ M2 macrophages were increased (30.7±2.7 vs 21.7±2.8, p = 0.03) compared to the control group. Paricalcitol also decreased TGF-β1 expression on day 30 (47.1±5.3 vs 70.8±7.1, p = 0.03) and MMP-9 on day 20 (28.9±2.5 vs 76.4±4.7, p < 0.001).</p><p><strong>Discussion: </strong>The present study investigates the effects of paricalcitol, a selective vitamin D receptor (VDR) agonist, on bleomycin-induced pulmonary fibrosis, revealing notable reductions in inflammatory and fibrotic markers. Our findings indicate that paricalcitol treatment (PF+P group) significantly attenuates fibrosis severity, as observed through histopathological, immunohistochemical, and molecular genetic analyses.</p><p><strong>Conclusion: </strong>Paricalcitol markedly reduces fibrosis severity, as shown through histopathological, immunohistochemical, and molecular genetic analyses. The treatment decreased the expression of key fibrotic and inflammatory markers, including TGF-β, MMP9, IL-1β, and TNF-α, and shifted macrophage polarization toward an anti-inflammatory M2 phenotype. These findings suggest paricalcitol's potential in modulating the immune response and highlight its therapeutic promise.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":"26 ","pages":"e18715303434362"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13629160/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149013540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Iodine Nutrition in Emilia-Romagna Region, Italy: A Successful Story of Prevention of Iodine Deficiency Disorders.","authors":"Domenico Meringolo, Daniela Rotondi, Davide Bianchi, Maria Dolores Scarfoglio, Giovanni Sorrenti, Angela Guaragna, Ramini Remo, Michele Mercuri, Michela Polazzi, Antonella Olivieri, Simona De Angelis","doi":"10.2174/0118715303427490260109050556","DOIUrl":"10.2174/0118715303427490260109050556","url":null,"abstract":"<p><p>The Emilia-Romagna region, Italy, achieved iodine sufficiency many years before the approval of Law 55/2005, which introduced a nationwide salt iodization program voluntarily in the country. Indeed, more than 10 years before the law, the Emilia-Romagna region implemented a local program of iodine, carrying out information campaigns to promote the use of iodized salt in the population. Epidemiological studies conducted between 1998 and 2005 in this region showed a progressive increase in the use of iodized salt (IS) and a median urinary iodine concentration >100 μg/L in almost all the investigated towns and villages. In 2005, when the national Law 55/2005 was approved, the prevalence of IS consumers in the Emilia-Romagna region was 60%, while it was only 30% in the rest of the country. Further studies conducted between 2011 and 2019 confirmed an adequate iodine intake in the population and the disappearance of goitre in schoolchildren, demonstrating the sustainability of the regional iodine prophylaxis program. Of note, the success obtained in this region is the result of a close collaboration between local politicians, health services, school authorities, families, and salt producers that, in the absence of dedicated funds, moved voluntarily to spread knowledge on the importance of using IS. Multiple and reiterated \"on-field\" initiatives experienced at the local level yielded awareness in the population on the importance of IS, suggesting that tight cooperation among stakeholders is successful in promoting large-scale programs of prevention.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":"e18715303427490"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13670184/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148261160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Celastrol Attenuates FGF23 Expression in Osteoblasts by Inhibiting STAT3 Activation.","authors":"Jiawei Cao, Yuewen Tang, Feng Wan, Tingjiao Xu, Ruchun Yang","doi":"10.2174/0118715303420913251205154844","DOIUrl":"10.2174/0118715303420913251205154844","url":null,"abstract":"<p><strong>Introduction: </strong>In this study, we aim to investigate the mechanism by which extracellular phosphate (Pi) regulates the transcription of fibroblast growth factor 23 (FGF23) in osteoblasts and the effects of celastrol on FGF23 expression in UMR-106 cells and in chronic kidney disease (CKD) rat models.</p><p><strong>Methods: </strong>We used Pi to induce FGF23 expression in a rat osteoblastic cell line as a model and then treated the cells with celastrol. The cytotoxicity of Pi and celastrol was assessed using the CCK-8 assay. FGF23 expression was measured using real-time quantitative PCR (RT-qPCR), and its promoter activity was evaluated using luciferase reporter assays. To detect active signal transducer and activator of transcription 3 (STAT3), immunofluorescence and Western blotting were performed. The 5/6 nephrectomized rat model was established to investigate the effects of celastrol on FGF23 expression <i>in vivo</i>. An enzyme-linked immunosorbent assay was carried out to examine serum FGF23 levels in rats. RT-qPCR detected the mRNA levels of FGF23 and STAT3 in the femurs of CKD rats.</p><p><strong>Results: </strong>We found that high Pi activated STAT3 and promoted its nuclear translocation, leading to elevated FGF23 expression, which was suppressed by celastrol. Additionally, in rats subjected to 5/6 nephrectomy with high serum Pi levels, serum FGF23 levels and skeletal STAT3 expression were significantly decreased after celastrol treatment.</p><p><strong>Discussion: </strong>Therefore, celastrol could have therapeutic effects on CKD by decreasing serum FGF23.</p><p><strong>Conclusion: </strong>High Pi activates STAT3 and induces FGF23 expression. Furthermore, celastrol can attenuate increased FGF23 expression induced by high Pi, potentially via inhibition of STAT3 activation.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":"e18715303420913"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13670194/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148379076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Mechanism of Icariin in Regulating BMSCs for Treating Osteoporosis: A Review.","authors":"Chengjie Wang, Zhenyu Wu, Yawei Xu, Yuyi Li, Zhenwei Man, Kang Liu, Jian Wang, Wenlin Lin, Fengqing Qie, Xiaolin Shi, Yifeng Yuan","doi":"10.2174/0118715303467650260722042115","DOIUrl":"10.2174/0118715303467650260722042115","url":null,"abstract":"<p><strong>Introduction: </strong>Osteoporosis (OP) is a common skeletal disease mainly caused by the imbalance between bone formation and bone resorption. Dysfunction and senescence of bone marrow mesenchymal stem cells (BMSCs) are critical pathogenic factors for OP, resulting in impaired osteogenic differentiation, increased adipogenic shift, and enhanced susceptibility to inflammation and oxidative stress. Therefore, the purpose of this review is to systematically synthesize current evidence on how Icariin (ICA)-a major bioactive flavonoid from <i>Epimedium</i> -exhibits therapeutic potential against OP by targeting BMSC senescence and regulating multiple underlying signaling networks.</p><p><strong>Methods: </strong>This narrative review systematically synthesized preclinical and mechanistic evidence regarding Icariin-mediated regulation of BMSC function in osteoporosis. Relevant cellular, animal, pharmacological, and mechanistic studies were reviewed, with emphasis on BMSC senescence, osteogenic/ adipogenic lineage commitment, oxidative stress, inflammation, and major signaling pathways, including Wnt/β-catenin, Notch, BMP/Runx2/Osx, MAPK, and OPG/RANK/RANKL.</p><p><strong>Results: </strong>ICA can promote osteogenic differentiation and inhibit osteoclastogenesis by regulating multiple signaling pathways simultaneously. ICA activates the Wnt/β-catenin pathway to enhance the stability of β-catenin and its downstream transcriptional programs, modulates Notch signaling through regulating the activity of DLL1, Jagged1, and NICD, and promotes the BMP/Runx2/Osx axis, which favors osteoblast lineage commitment. Additionally, it controls the activity of MAPK (ERK, p38, JNK) and restores bone homeostasis by managing the OPG/RANK/RANKL system, leading to reduced osteoclastogenesis and decreased production of inflammatory cytokines. In addition to regulating lineage commitment, ICA alleviates BMSC senescence by reducing oxidative stress, DNA damage, mitochondrial dysfunction, and SASP-associated microenvironmental deterioration.</p><p><strong>Discussion: </strong>Collectively, these effects promote osteogenesis, maintain stem cell vitality, and mitigate OP-induced bone loss. The hierarchy, crosstalk, and cell-type specificity of ICA-targeted signaling networks require further elucidation to facilitate clinical translation.</p><p><strong>Conclusion: </strong>Preclinical evidence suggests ICA is a promising natural compound with the potential to mitigate OP progression by comprehensively regulating BMSC functions and bone remodeling pathways. Future research needs to focus on rigorous clinical trials and single-cell-level studies to determine the specific BMSC subpopulations responsive to ICA and optimize its therapeutic application.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":"e18715303467650"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13659195/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148709206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clopidogrel-Induced Insulin Autoimmune Syndrome: Efficacy of Glucocorticoid Therapy and Continuous Glucose Monitoring.","authors":"Lihui Luo, Xiaoqing Xiong, Jianmin Ran","doi":"10.2174/0118715303394353250727192242","DOIUrl":"10.2174/0118715303394353250727192242","url":null,"abstract":"<p><strong>Introduction: </strong>Insulin autoimmune syndrome (IAS) is a rare cause of spontaneous hyperinsulinemic hypoglycemia characterized by elevated insulin autoantibody (IAA). Over half of IAS cases involve exposure to sulfhydryl group-containing medications or their active metabolites, with clopidogrel being an uncommon trigger. We report a case of clopidogrel-induced IAS (CIAS) treated with glucocorticoid and managed by continuous glucose monitoring (CGM) during follow-up.</p><p><strong>Case report: </strong>A 77-year-old man developed recurrent severe hypoglycemia events after receiving clopidogrel for six months. Laboratory investigations showed significantly elevated serum insulin levels (peak: 1,452.52 mIU/L; normal range: 1.9-23.0 mIU/L) and a high IAA titer of 37.0 COI (>1.1 COI, positive). Following the exclusion of other potential causes of hypoglycemia, IAS was diagnosed. Consequently, clopidogrel was discontinued, and combination therapy incorporating prednisolone was initiated. During the 10-month follow-up, insulin levels declined to 8.09 mIU/L with IAA titers decreasing to 1.35 COI. Analysis of CGM data demonstrated a transition from glycemic fluctuations to stabilization.</p><p><strong>Conclusion: </strong>This single-patient case report highlights the significance of identifying CIAS as a rare adverse effect of a drug, the effectiveness of glucocorticoid therapy, and the role of CGM in IAS management.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":"e18715303394353"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13662727/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144857337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the Therapeutic Potential and Safety Profile of <i>Tripterygium wilfordii</i> Hook.f. in Osteoarthritis: Mechanisms, Toxicity, and Clinical Perspectives.","authors":"Jianpeng Zhao, Xingyan Ma, Yanxia Yin, Xin Zhang, Mengyang Zheng, Jing Yang, Weiguo Wang","doi":"10.2174/0118715303454168260516214848","DOIUrl":"10.2174/0118715303454168260516214848","url":null,"abstract":"<p><strong>Introduction: </strong><i>Tripterygium wilfordii Hook.f.</i> (TwHF), A traditional Chinese medicine has been historically used for treating inflammatory conditions such as osteoarthritis (OA) and rheumatoid arthritis (RA), owing to its potent anti-inflammatory and immunomodulatory properties. Notably, OA is now recognized as a whole-joint disorder driven not merely by mechanical wear and tear, but by complex pathophysiological processes involving immune response dysregulation and localized metabolic disturbances. Despite its therapeutic potential, the clinical application of TwHF remains constrained by significant multi-organ toxicity and a narrow therapeutic window. This review aims to summarize the therapeutic mechanisms, toxicity profile, and clinical evidence of TwHF and its active components in OA treatment, and to discuss strategies for mitigating toxicity and future research directions.</p><p><strong>Methods: </strong>A systematic search was performed across multiple electronic databases, including PubMed and Web of Science, up to February 2026, to identify studies on TwHF and its components in OA. The process followed PRISMA guidelines using keywords including \"Tripterygium wilfordii,\" \"osteoarthritis,\" and \"toxicity.\" Included studies focused on TwHF and OA pharmacology, toxicity, or clinical outcomes; those with insufficient data were excluded. Data on authors, year, findings, and conclusions were extracted and synthesized narratively by themes.</p><p><strong>Results: </strong>TwHF active components demonstrate potent anti-inflammatory and chondroprotective effects in cellular and animal OA models. However, they also cause dose-dependent hepatotoxicity, nephrotoxicity, and immunosuppression. Strategies like drug combination, targeted delivery, and metabolic modulation can reduce toxicity. Clinical evidence in OA remains limited and lowquality, whereas more robust data support its use in rheumatoid arthritis.</p><p><strong>Discussion: </strong>TwHF presents a compelling therapeutic profile for OA due to its multi-faceted anti- inflammatory and immunomodulatory actions, primarily mediated by its active constituents through a multi-targeted approach. However, its promise is tempered by significant safety concerns, particularly hepatotoxicity and nephrotoxicity, and a lack of conclusive efficacy data from robust clinical trials in OA.Future research should prioritize high-quality RCTs, deeper investigation into toxicity mechanisms, development of safer derivatives, and establishment of predictive biomarkers.</p><p><strong>Conclusion: </strong>While TwHF holds promise for OA treatment due to its multimodal anti-inflammatory mechanisms, its toxicity and insufficient clinical evidence necessitate further high-quality trials, precise therapeutic targeting, and safer formulation development for safe clinical integration.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":"e18715303454168"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148709235","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 Evolution of Pediatric MAFLD Research (2014-2023): A Decade-Long Bibliometric Analysis of Emerging Trends","authors":"Tianyi Li, Xiaoying Zhang, Daojun Wang, Lixia Zhang, Qiong Wu, Wei Yan, Fengfeng Cui, Mengyao Huang, Peng Hua, Xiang Cui","doi":"10.2174/0118715303404437250611123553","DOIUrl":"10.2174/0118715303404437250611123553","url":null,"abstract":"<p><strong>Background: </strong>Metabolic dysfunction-related fatty liver disease (MAFLD) has emerged as the predominant chronic liver disorder among children and adolescents. Like in adults, pediatric MAFLD encompasses a disease spectrum progressing from isolated steatosis to inflammatory changes, fibrotic development, and ultimately, cirrhosis. Despite increasing recognition of MAFLD as a major pediatric health issue, current literature lacks a systematic quantitative evaluation of research trends, leading to knowledge gaps in this field. To address this limitation, a comprehensive bibliometric analysis was performed to assess global research output on pediatric MAFLD by focusing specifically on the 2014-2023 period. This analysis avoids the confounding effects of the heterogeneity of earlier data while achieving sufficient temporal resolution to reveal emerging trends that might be obscured in long-term studies. This study synthesizes existing evidence, enhances understanding of this disciplinary field, and informs future research directions in pediatric MAFLD.</p><p><strong>Methods: </strong>Articles concerning children with MAFLD published from 2014--2023 were identified from the Science Citation Index-Expanded of the Web of Science Core Collection. CiteSpace software, VOSviewer, and the Online Analysis Platform of Literature Metrology were used to analyze the current publication trends and hotspots.</p><p><strong>Results: </strong>The analysis identified 1,609 English-language articles on pediatric MAFLD published from 2014 to 2023. The United States emerged as the most active participant in international collaborations. The University of California San Diego (UCSD) demonstrated the highest research output among the analyzed institutions. Additionally, UCSD exhibited the most extensive collaborative network, engaging in frequent and substantive research partnerships with a diverse range of academic and scientific organizations. Valerio Nobili was found to be the most prolific author, with 67 articles. Keyword burst analysis revealed that cardiovascular risk factors were the most intense research hotspot.</p><p><strong>Conclusion: </strong>Current research on pediatric MAFLD warrants greater attention, particularly regarding cardiovascular risk factors. This study provides valuable references for researchers, offering insights to guide future research directions and potential collaborations.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":"e18715303404437"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13334261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144586053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of the Space GlucoseControl System for Managing Stress-Induced Hyperglycemia in ICU Patients: Efficacy and Safety Assessment","authors":"Peng-Cheng Liu, Dan-Dan Fan, Qun-Ying Bao, Xiao-Mei Jiang, Juan Lu","doi":"10.2174/0118715303346311250415111740","DOIUrl":"10.2174/0118715303346311250415111740","url":null,"abstract":"<p><strong>Background: </strong>Despite the increasing adoption of the Space GlucoseControl system (SGCs), a novel blood glucose management technique, in critically ill patients, its efficacy and safety warrant further investigation.</p><p><strong>Objective: </strong>This study aimed to assess the efficacy and safety of SGCs in managing patients with stress-induced hyperglycemia in the intensive care unit.</p><p><strong>Methods: </strong>A prospective study was conducted involving 22 patients with stress-induced hyperglycemia monitored using the SGCs for 72 hours. Measurements included mean blood glucose, maximum blood glucose, minimum blood glucose, and frequencies of hyperglycemia (> 8.3 mmol/L), hypoglycemia (< 4.4 mmol/L), and target blood glucose (4.4 - 8.3 mmol/L).</p><p><strong>Results: </strong>Mean blood glucose level was significantly different at 24 hours and 48 hours and 24 hours and 72 hours with SGCs (24h vs 48h, P=0.0289; 24h vs 72h, P=0.0252). The times of hyperglycemia (> 8.3 mmol/L) (24h vs 48h, P=0.0289; 24h vs 72h, P=0.0216) was significantly reduced at 48 hours and 72 hours compared to 24 hours. The average interval between blood glucose measurements was significantly extended at 48 hours and 72 hours compared to 24 hours (24h vs 48h, P=0.0037; 24h vs 72h, P=0.0332). The frequency of target blood glucose (4.4 - 8.3 mmol/L) under SGCs blood glucose management at 48 hours and 72 hours was significantly higher than at 24 hours (24h vs 48h, P=0.0395; 24h vs 72h, P=0.0379). There was no significant difference in the times of hypoglycemia (< 4.4 mmol/L) and the highest blood glucose values between 24 hours, 48 hours, and 72 hours with SGCs glucose management (P>0.05). These findings indicate that SGCs blood glucose management can promote greater stability in the blood glucose levels of patients and alleviate the workload of medical staff to some extent.</p><p><strong>Conclusion: </strong>SGCs is effective in stabilizing blood glucose levels, increasing the frequency of target blood glucose values, and thereby reducing significant glucose fluctuations, which can improve patient recovery outcomes. Additionally, prolonged use of the SGCs not only optimizes glucose management but also significantly alleviates the workload of nursing staff, enhancing efficiency and allowing for more focused patient care.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":"e18715303346311"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13284663/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144056357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unlocking New Treatment Horizons for Celiac Disease: PRKCD Revealed as a Promising Target through Mendelian Randomization","authors":"Jie Zhou, Yixin Xu, Haitao Wang, Kun Wang, Chao Chen","doi":"10.2174/0118715303410531250815124524","DOIUrl":"10.2174/0118715303410531250815124524","url":null,"abstract":"<p><strong>Introduction: </strong>Celiac Disease (CeD) is a serious, lifelong autoimmune condition. There remains a significant unmet medical need for effective pharmacological treatments for CeD.</p><p><strong>Methods: </strong>We utilized summary statistics for 2,888 druggable genes from the eQTLGen Consortium and the FinnGen Consortium for CeD. In our Mendelian Randomization (MR) analysis, we identified genes associated with CeD that had a false discovery rate (FDR) < 0.05 using the Inverse Variance Weighted (IVW) method. To enhance the reliability of the results, we validated them through colocalization analysis and Summary-data-based Mendelian Randomization (SMR) analyses.</p><p><strong>Results: </strong>Through our analysis, we identified 18 druggable genes with a causal relationship to CeD under an FDR < 0.05. Subsequent colocalization and SMR analyses highlighted the PRKCD gene as a potential therapeutic target for CeD (IVW method: Odds Ratio 1.319, 95% Confidence Interval 1.182-1.471, P = 6.85E-07, FDR = 0.002). Additionally, these results have passed horizontal pleiotropy tests, heterogeneity analysis, and leave-one-out sensitivity analysis.</p><p><strong>Discussion: </strong>The identification of PRKCD as a therapeutic target represents a significant advancement in addressing the unmet medical need for CeD treatment. However, the hypothesis that PRKCD contributes to CeD pathogenesis by regulating tight junction proteins and altering intestinal barrier function requires further experimental validation in future studies.</p><p><strong>Conclusion: </strong>Our study is the first to identify the PRKCD gene as a potential therapeutic target for treating CeD, providing new insights into the treatment of CeD and guiding the development of corresponding therapeutic drugs.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":"e18715303410531"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13284647/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145002479","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bibliometric Analysis of Emerging Trends and Hotspots in the Links between Nonalcoholic Steatohepatitis and Diabetes Mellitus from 2004 to 2023.","authors":"Chen Xie, Tao Liu, Yuanxin Zhong, Zhengyu Li, Ji Xu, Zijun Zhao, Xinqiang Wang, Po Gao","doi":"10.2174/0118715303396313250904204350","DOIUrl":"10.2174/0118715303396313250904204350","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;In recent years, the prevalence of nonalcoholic steatohepatitis (NASH) has been rising globally. NASH has been linked to liver fibrosis, cirrhosis, hepatocellular carcinoma (HCC), and liver transplantation (LT), with the progression and severity of NASH closely impacting patients' prognosis. This increasing incidence highlights the urgent need for effective therapeutic strategies and early detection methods to mitigate the progression of the disease and improve patient prognosis. Accumulating evidence indicates that NASH and diabetes mellitus (DM) are interconnected and mutually affect each other. This study utilized bibliometric analysis to assess current publication trends and focal points in the links between NASH and DM, aiming to promote research in this area.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;We thoroughly searched the Science Citation Index-Expanded (SCI-E) of the Web of Science Core Collection (WoSCC), PubMed, and the Excerpta Medica Database (Embase) to identify relevant articles on the links between NASH and DM from 2004 to 2023. The current publication trends and hotspots in this field were analyzed using the Online Analysis Platform of Literature Metrology, CiteSpace software, VOSviewer, and the R package Bibliometrix.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;From 2004 to 2023, 943 articles were found that focused on the links between NASH and DM with a noticeable surge in publications since 2015. The United States has taken the primary position in terms of the number of publications. It has also been the most active country in international collaborative efforts. The University of California, San Diego, and Kenneth Cusi were the most productive institution and scholar, respectively. The co-citation keywords cluster labels revealed 10 primary clusters: adiponectin, MAFLD, mortality, NASH, nonalcoholic fatty liver, SGLT2, neurodegeneration, LY2405319, autophagy, and hepatocytes. Recent studies focused on weight loss, fibrosis stage, NAFLD, mortality, and diabetes mellitus.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Discussion: &lt;/strong&gt;Research on NASH and DM has transitioned from early mechanistic exploration to a current focus on weight management, diabetes control, and fibrosis prevention, particularly through lifestyle interventions and antidiabetic drug therapy. Future studies should integrate lifestyle adjustments with drug development, enhance international cooperation to fill regional research gaps, and achieve more effective management of NASH and DM.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;Over the past 20 years, global publications on the relationship between NASH and DM have grown rapidly. The current research hotspots focus on weight loss, and the reduction of blood glucose and fibrosis in NASH. Maintaining a healthy diet, exercising regularly, taking appropriate medication, and being vigilant about complications are essential for delaying the progression of NASH and DM. These are also the primary future directions of research.&lt;/p&gt;&lt;p","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":"e18715303396313"},"PeriodicalIF":2.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13358780/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145115888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}