Journal of molecular endocrinology最新文献

OGT accelerates diabetic retinopathy via O-GlcNAcylation of BAP1. OGT通过o - glcn酰化BAP1加速糖尿病视网膜病变。

IF 3.8 4区医学

Journal of molecular endocrinology Pub Date : 2026-05-07 DOI: 10.1530/JME-25-0065

Bairong Wang, Junteng Yao, Yuren Zhang, Meirong Li, Jinting Xu, Yinan Chen, Yiping Zhang, Qiaolan Liu, Xiaoting Li

{"title":"OGT accelerates diabetic retinopathy via O-GlcNAcylation of BAP1.","authors":"Bairong Wang, Junteng Yao, Yuren Zhang, Meirong Li, Jinting Xu, Yinan Chen, Yiping Zhang, Qiaolan Liu, Xiaoting Li","doi":"10.1530/JME-25-0065","DOIUrl":"https://doi.org/10.1530/JME-25-0065","url":null,"abstract":"Diabetic retinopathy (DR), a prevalent neurovascular complication of diabetes, is a leading cause of blindness in affected individuals. O-linked β-D-N-acetylglucosamine modification (O-GlcNAcylation), a unique form of post-translational modification regulated by O-GlcNAc transferase (OGT) and O-GlcNAcase, plays a critical role in cellular processes. This study aimed to investigate the role of OGT-mediated O-GlcNAcylation and its potential regulatory mechanisms in DR. Using a DR mouse model, we evaluated the effect of OGT on retinal tissue damage. An in vitro model was established by treating human retinal endothelial cells (HRECs) with high glucose (HG). The biological behaviors of HRECs were assessed using cell counting kit-8, EdU incorporation, transwell, and tube formation assays. Underlying mechanisms were explored through quantitative real-time PCR, Western blot, and co-immunoprecipitation. Our findings revealed that O-GlcNAcylation levels were significantly elevated both in vitro and in vivo. Knockdown of OGT suppressed the proliferation, migration, and angiogenesis of HG-stimulated HRECs, an effect mediated through the upregulation of BAP1. Mechanistically, OGT was found to interact with BAP1 and promote its O-GlcNAcylation, thereby negatively regulating BAP1 expression. Furthermore, OGT knockdown attenuated retinal tissue damage in diabetic mice, an effect dependent on BAP1. In summary, this study reveals a novel role for OGT-mediated O-GlcNAcylation in DR progression, suggesting its potential as a therapeutic target for DR.","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856506","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

Thyroglobulin and Thyroglobulin Antibodies in Differentiated Thyroid Cancer: Interpretation, Challenges and Future Perspectives. 分化型甲状腺癌中的甲状腺球蛋白和甲状腺球蛋白抗体：解释、挑战和未来展望。

IF 3.8 4区医学

Journal of molecular endocrinology Pub Date : 2026-04-28 DOI: 10.1530/JME-25-0217

M H Links, T P Links, W T Zandee, A C Muller Kobold

{"title":"Thyroglobulin and Thyroglobulin Antibodies in Differentiated Thyroid Cancer: Interpretation, Challenges and Future Perspectives.","authors":"M H Links, T P Links, W T Zandee, A C Muller Kobold","doi":"10.1530/JME-25-0217","DOIUrl":"https://doi.org/10.1530/JME-25-0217","url":null,"abstract":"Thyroglobulin (Tg) is a thyroid-specific protein playing a key role in thyroid hormone production. For patients with differentiated thyroid carcinoma (DTC), Tg is the main biomarker during follow-up determining treatment response and risk of disease recurrence. Accurate Tg measurement is complicated by assay-specific performance and interference, most notably thyroglobulin autoantibodies (TgAbs). High-sensitivity Tg assays can detect very low Tg levels, eliminating the need for TSH-stimulated Tg-measurements. Because of potential TgAb interference in Tg assays, TgAb measurement must always accompany Tg analysis. TgAbs are present in a minority of healthy individuals, but in up to one third of patients with DTC. While low-level TgAbs are often clinically irrelevant, higher titers interfere with Tg immunoassays, possibly causing false-negative Tg results. Importantly, TgAb trends themselves provide prognostic information: declining concentrations support remission, whereas rising titers may indicate recurrence, offering a potential useful surrogate marker when Tg is unreliable. Alternative and complementary laboratory strategies are emerging. Novel proteomic approaches may allow isoform-specific Tg detection, potentially distinguishing tumour-derived Tg from normal Tg. In parallel, liquid biopsy technologies, particularly cell-free DNA, circulating tumour DNA and microRNA assays, are being explored for non-invasive detection of minimal residual disease, though their role in DTC remains to be defined. In summary, Tg and TgAbs remain the mainstay of laboratory monitoring in DTC. Their interpretation demands awareness of assay limitations, appropriate cut-offs, and the clinical context. Future integration of advanced proteomic and genomic biomarkers holds promise for more specific, individualized surveillance strategies in thyroid cancer.","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147774247","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

Integrating mechanistic models to decode the GnRH pulse generator in female mice. 整合机制模型解码雌性小鼠GnRH脉冲发生器。

IF 3.8 4区医学

Journal of molecular endocrinology Pub Date : 2026-04-28 Print Date: 2026-04-01 DOI: 10.1530/JME-25-0224

Kateryna Nechyporenko, Deyana Ivanova, Xiao Feng Li, Krasimira Tsaneva-Atanasova, Margaritis Voliotis, Kevin T O'Byrne

{"title":"Integrating mechanistic models to decode the GnRH pulse generator in female mice.","authors":"Kateryna Nechyporenko, Deyana Ivanova, Xiao Feng Li, Krasimira Tsaneva-Atanasova, Margaritis Voliotis, Kevin T O'Byrne","doi":"10.1530/JME-25-0224","DOIUrl":"10.1530/JME-25-0224","url":null,"abstract":"The gonadotrophin-releasing hormone (GnRH) pulse generator is a critical neural oscillator that governs reproductive function through the pulsatile release of luteinising hormone (LH) and follicle-stimulating hormone. Early electrophysiological studies, notably by Ernst Knobil, identified multiunit activity (MUA) volleys in the mediobasal hypothalamus that aligned with LH pulses, suggesting a neural basis for GnRH pulsatility. Although GnRH neurons exhibit some intrinsic secretory rhythmicity in vitro, their isolated electrophysiological signatures have proven inconsistent. Recent advances, including GCaMP fibre photometry in freely behaving mice, have revealed a precise correlation between episodic GnRH distal process activity and LH pulses. However, it is now well established that a neural oscillator comprising hypothalamic kisspeptin neurones co-expressing neurokinin B and dynorphin, collectively termed the KNDy network, represents the core construct of the GnRH pulse generator. Understanding the dynamics of this network and its modulation by external inputs, such as stress, metabolic cues and circadian rhythms, is essential. Computational modelling provides a systematic framework for integrating experimental data with mechanistic and predictive analyses to decode the GnRH pulse generator dynamics.","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13150289/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147690805","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

Adsorption represents a critical challenge in the quantification of free 25-hydroxyvitamin D3. 吸附是定量游离25-羟基维生素D3的一个关键挑战。

IF 3.8 4区医学

Journal of molecular endocrinology Pub Date : 2026-04-27 Print Date: 2026-04-01 DOI: 10.1530/JME-25-0207

Nick Narinx, Tom De Waal, Jennifer Afrakoma Nyamaah, Karel David, Joeri Walravens, Tom Fiers, Bruno Lapauw, Brigitte Decallonne, Frank Claessens, Jaak Billen, Dirk Vanderschueren, Pieter Vermeersch, Leen Antonio

{"title":"Adsorption represents a critical challenge in the quantification of free 25-hydroxyvitamin D3.","authors":"Nick Narinx, Tom De Waal, Jennifer Afrakoma Nyamaah, Karel David, Joeri Walravens, Tom Fiers, Bruno Lapauw, Brigitte Decallonne, Frank Claessens, Jaak Billen, Dirk Vanderschueren, Pieter Vermeersch, Leen Antonio","doi":"10.1530/JME-25-0207","DOIUrl":"10.1530/JME-25-0207","url":null,"abstract":"Equilibrium dialysis followed by liquid chromatography-tandem mass spectrometry is considered the gold standard for the isolation and quantification of free hormones. However, this technique has not been described for the analysis of free 25-hydroxyvitamin D3. This study investigated analytical challenges, focusing on stability and adsorption of 25-hydroxyvitamin D3 in aqueous buffer environments, to be considered prior to method development of equilibrium dialysis for free vitamin D. Experiments revealed that 25-hydroxyvitamin D3 is highly prone to adsorption, and to a minor extent degradation, resulting in severe analyte loss already upon introduction of 25-hydroxyvitamin D3 into the aqueous environment, far exceeding observations in serum where protein binding provides significant protection. While chemical degradation only slightly contributes, strong surface adsorption accounts for the majority of 25-hydroxyvitamin D3 loss observed. In contrast, the addition of methanol to the buffer environment completely mitigated analyte loss, confirming the severe adsorption of 25-hydroxyvitamin D3 to recipient surfaces. However, incorporating methanol as a buffer component fundamentally altered experimental conditions, thereby potentially disrupting the physiological equilibrium between 25-hydroxyvitamin D3, vitamin D-binding protein, and albumin, and by extension the free fraction of vitamin D. Consequently, the large extent of, primarily, adsorption of 25-hydroxyvitamin D3 in aqueous environments represents an important consideration in setting up equilibrium dialysis experiments for free vitamin D. These findings additionally highlight a critical need for novel analytical strategies that prevent adsorption while maintaining physiological equilibrium in the assessment of free vitamin D.","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147690769","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

Protective effect of pentoxifylline against high-glucose-induced ferroptosis in vascular smooth muscle cells. 己酮可可碱对高糖诱导的血管平滑肌细胞铁下垂的保护作用。

IF 3.8 4区医学

Journal of molecular endocrinology Pub Date : 2026-04-24 Print Date: 2026-04-01 DOI: 10.1530/JME-25-0086

Jing Zhou, Lijing Jiao, Siyao Jin, Yiwei Ran, Xian Meng, Lu Bai, Yanru Xi, Jing Wang, Zhansheng Zhao

{"title":"Protective effect of pentoxifylline against high-glucose-induced ferroptosis in vascular smooth muscle cells.","authors":"Jing Zhou, Lijing Jiao, Siyao Jin, Yiwei Ran, Xian Meng, Lu Bai, Yanru Xi, Jing Wang, Zhansheng Zhao","doi":"10.1530/JME-25-0086","DOIUrl":"10.1530/JME-25-0086","url":null,"abstract":"Graphical abstract: Abstract: Ferroptosis has emerged as a pivotal form of regulated cell death implicated in diabetic vascular complications, yet the upstream transcriptional mechanisms governing this process remain insufficiently defined. Chronic hyperglycemia induces oxidative stress, iron overload, and vascular remodeling, but how these metabolic disturbances trigger ferroptotic signaling in vascular smooth muscle cells (VSMCs) remains unclear. In this study, we identify Krüppel-like factor 10 (KLF10) as a critical transcriptional mediator linking hyperglycemia to ferroptotic activation in VSMCs. High glucose increased KLF10 expression and enhanced its binding to the GPX4 promoter, leading to transcriptional repression of GPX4, heightened lipid peroxidation, and elevated reactive oxygen species. Pentoxifylline (PTX), a clinically used hemorheologic agent with antioxidant properties, significantly reduced ferroptosis-related lipid accumulation and partially restored GPX4 expression by suppressing KLF10 in vitro. In diabetic mice, PTX similarly attenuated dysregulation of the KLF10/GPX4 axis, lowered iron deposition, improved antioxidant enzyme activity, and mitigated vascular remodeling. Collectively, these findings establish the KLF10/GPX4 axis as a previously unrecognized regulator of diabetes-associated vascular ferroptosis and suggest that PTX may offer a promising therapeutic approach for limiting ferroptosis-driven vascular injury in diabetes.","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13130825/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147592818","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

SfE BES 2026: What's new in basic science endocrinology? SfE BES 2026：基础科学内分泌学有什么新进展？

IF 3.8 4区医学

Journal of molecular endocrinology Pub Date : 2026-04-24 Print Date: 2026-04-01 DOI: 10.1530/JME-26-0062

Gabriela da Silva Xavier

引用次数: 0

The Molecular Mechanism of Melatonin in Regulating Osteoporosis Based on the RANKL/OPG Signaling Axis. 基于RANKL/OPG信号轴的褪黑素调节骨质疏松的分子机制

IF 3.8 4区医学

Journal of molecular endocrinology Pub Date : 2026-04-22 DOI: 10.1530/JME-25-0220

Tai Guo, Junqing Jia, Dongsheng Hao, Peng Hu, Lin Sun

{"title":"The Molecular Mechanism of Melatonin in Regulating Osteoporosis Based on the RANKL/OPG Signaling Axis.","authors":"Tai Guo, Junqing Jia, Dongsheng Hao, Peng Hu, Lin Sun","doi":"10.1530/JME-25-0220","DOIUrl":"https://doi.org/10.1530/JME-25-0220","url":null,"abstract":"Melatonin is a promising drug for improving bone mass in postmenopausal women. This study investigated the mechanism behind the regulation of melatonin on osteoblast differentiation. Mouse embryonic osteoblast precursor MC3T3-E1 cells were treated with melatonin or transfected with cathepsin D (CTSD) vectors. A cellular model was established by H2O2 treatment. Alkaline phosphatase (ALP) staining and Alizarin Red S staining were performed. An osteoporosis mouse model was established by ovariectomy (OVX) and treated with melatonin or transfected with a CTSD knockdown vector. Bone biomechanical testing was performed to assess bone strength. Histological bone damage was assessed, osteoclast differentiation was visualized using tartrate resistant acid phosphatase staining, osteocalcin (OCN) and type I collagen α1 chain (COL1A1) expression was visualized using immunohistochemistry, and serum bone turnover markers procollagen type I N-propeptide (PINP) and C-terminal telopeptide of type I collagen (CTX-1) levels were measured using enzyme-linked immunosorbent assay. Receptor activator of NF-κB ligand (RANKL), osteoprotegerin (OPG), Wnt3a, and β-catenin protein levels were determined using western blotting. Melatonin treatment or CTSD overexpression promoted ALP activity and mineralization in MC3T3-E1 cells. Melatonin upregulated CTSD expression. Melatonin treatment enhanced bone strength, inhibited osteoclast differentiation, increased OCN and COL1A1 expression, elevated PINP levels, and reduced CTX-1 in OVX mice. Moreover, melatonin suppressed RANKL expression and promoted OPG, Wnt3a, and β-catenin expression. CTSD knockdown abolished the regulatory effects of melatonin on MC3T3-E1 cells and OVX mice. In conclusion, melatonin increases CTSD expression to promote osteoblast differentiation and regulate the RANKL/OPG/Wnt signaling pathway, thereby slowing down the progression of osteoporosis.","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147774204","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

Metabolic-renal disease genetic architecture revealed by genomic structural equation modeling. 基因组结构方程模型揭示的代谢性肾脏疾病遗传结构。

IF 3.8 4区医学

Journal of molecular endocrinology Pub Date : 2026-04-16 Print Date: 2026-04-01 DOI: 10.1530/JME-25-0171

Kaixi Ding, Li Xiang, Wei Jiang, Ming Lei, Yongxiang Gao

{"title":"Metabolic-renal disease genetic architecture revealed by genomic structural equation modeling.","authors":"Kaixi Ding, Li Xiang, Wei Jiang, Ming Lei, Yongxiang Gao","doi":"10.1530/JME-25-0171","DOIUrl":"10.1530/JME-25-0171","url":null,"abstract":"Physiologic mechanisms underlying metabolic and renal diseases interact and are highly comorbid, yet their genetic associations and underlying mechanisms have not been systematically elucidated. Using genome-wide association study (GWAS) summary statistics from UK Biobank, FinnGen, and CKDGen, we integrated and analyzed gout, serum urate, chronic kidney disease, kidney stones, and metabolic syndrome. Using genomic structural equation modeling (GSEM), we created the first genetic linkage map for 'gout-urate-kidney-metabolism' (GUKM) to explore shared genetic architecture. Post-GWAS analyses for GUKM-GSEM GWAS, including functional annotation, enrichment, fine-mapping, causal inference, and gsMap, identified key genetic loci, pathways, tissues/cell types, and potential drug targets. We identified 164 lead SNPs, including rs1260326 (chr2) and rs73607783 (chr8), with GSEA showing significant enrichment of GUKM-GSEM GWAS in cholesterol metabolism and lipid pathways (adjP < 0.05). Tissue and cell enrichment highlighted the liver, renal cortex, pancreas, proximal tubular epithelial cells, and hepatocytes (P < 0.05). Mendelian randomization indicated a potential causal role of GCKR (FDR < 0.05), which gsMap showed to be highly expressed in hepatocytes and liver tissue. The present study revealed the common genetic basis of metabolic and renal diseases and emphasized that lipid metabolism may be a key intermediary pathway connecting the 'metabolic-renal axis'. The liver, renal cortex, and pancreas were the primary enriched tissues, and GCKR was identified as a core gene and potential drug target. Overall, this study provides an important reference for the genetic mechanisms, key mechanisms, and intervention targets of related diseases.","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147592875","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

Cardiolipin alleviates insulin resistance by ameliorating mitochondrial dysfunction and promoting fatty acid oxidation. 心磷脂通过改善线粒体功能障碍和促进脂肪酸氧化来减轻胰岛素抵抗。

IF 3.8 4区医学

Journal of molecular endocrinology Pub Date : 2026-04-15 Print Date: 2026-04-01 DOI: 10.1530/JME-25-0103

Chengcheng Yao, Jianglan Long, Yueyue Wang, Xiaojia Liu, Tingting Qiu, Kuan Chen, Dan Yan

{"title":"Cardiolipin alleviates insulin resistance by ameliorating mitochondrial dysfunction and promoting fatty acid oxidation.","authors":"Chengcheng Yao, Jianglan Long, Yueyue Wang, Xiaojia Liu, Tingting Qiu, Kuan Chen, Dan Yan","doi":"10.1530/JME-25-0103","DOIUrl":"10.1530/JME-25-0103","url":null,"abstract":"Cardiolipin deficiency is closely associated with mitochondrial dysfunction and metabolic disorders, yet whether it directly modulates insulin resistance remains unknown. Here, we examined the effects of cardiolipin supplementation on insulin resistance and the underlying mechanisms using male C57BL/6J mice fed a high-fat diet, male db/db mice, and dexamethasone-induced insulin-resistant HepG2 cells, a well-established model for investigating hepatic insulin signaling. Intragastric administration of cardiolipin at 5 mg/kg lowered blood glucose, reduced weight gain, improved insulin sensitivity, and alleviated hepatic lipid accumulation in mice, along with decreased serum interleukin-6 and low-density lipoprotein cholesterol levels. Cardiolipin reduced the LC3-II/LC3-I ratio and Tom20 expression in both liver tissue and insulin-resistant HepG2 cells, indicative of enhanced mitophagy. In HepG2 cells, it also attenuated mitochondrial fragmentation, improved mitochondrial membrane potential, lowered reactive oxygen species production, and upregulated the expression of CPT1A and ACAD1. These findings demonstrate that cardiolipin mitigates hepatic insulin resistance by enhancing mitophagy and fatty acid oxidation, representing a promising therapeutic approach for insulin resistance-related metabolic disorders.","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147592864","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

Decoding the molecular landscape of the placenta in maternal diabetes: a systematic review of high-throughput data. 解码胎盘在母体糖尿病中的分子景观：高通量数据的系统回顾。

IF 3.8 4区医学

Journal of molecular endocrinology Pub Date : 2026-04-10 Print Date: 2026-04-01 DOI: 10.1530/JME-25-0131

Georgia Fakonti, Abigail R Byford, Eleanor M Scott, Beth Holder, Karen Forbes

{"title":"Decoding the molecular landscape of the placenta in maternal diabetes: a systematic review of high-throughput data.","authors":"Georgia Fakonti, Abigail R Byford, Eleanor M Scott, Beth Holder, Karen Forbes","doi":"10.1530/JME-25-0131","DOIUrl":"10.1530/JME-25-0131","url":null,"abstract":"Diabetes in pregnancy is associated with significant short- and long-term complications for mothers and offspring, many of which are thought to result from altered placental development and function. Although studies have demonstrated molecular changes in the placenta in this context, the precise mechanisms remain unclear. High-throughput transcriptomic and proteomic approaches provide powerful tools to systematically identify disease-associated pathways, yet no systematic synthesis of this literature has been undertaken. We conducted a systematic review of omics studies examining placental molecular changes in pregnancies complicated by diabetes compared with uncomplicated pregnancies. Fifty-six studies were eligible for inclusion, the majority of which focused on gestational diabetes mellitus (GDM; n = 52). Of these, 42 reported changes in RNA (n = 30) or protein (n = 12) abundance, with eight proteins and 189 RNA species consistently altered in at least two studies. Functional enrichment analysis revealed dysregulation of immune, vascular, and developmental pathways. Notably, 98 molecules were altered at both RNA and protein levels, 47 with consistent directionality across studies, suggesting robust disruption of core biological pathways. Comparisons across diabetes types showed partial overlap of differentially expressed transcripts between GDM and type 1 diabetes (16 genes) and GDM and type 2 diabetes (34 genes), although no universal markers were identified. These findings highlight shared molecular signatures in GDM, provide novel insights into pathways linking maternal diabetes to placental dysfunction and adverse outcomes, and emphasise the need for further studies on type 1 and type 2 diabetes. These pathways may represent potential therapeutic targets to mitigate intergenerational cardiometabolic risk.","PeriodicalId":16570,"journal":{"name":"Journal of molecular endocrinology","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13097123/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147467911","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