JOURNAL OF MOLECULAR ENDOCRINOLOGY分子内分泌学杂志
JOURNAL OF MOLECULAR ENDOCRINOLOGY(英文缩写 J MOL ENDOCRINOL),ISSN 0952-5041,eISSN 1479-6813,中文译名:分子内分泌学杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-10-01 至 2026-09-30，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 4.869 | Q2 |
| 2022 | 3.500 | Q3 |
| 2023 | 3.600 | Q2 |
| 2024 | 3.800 | Q2 |
| 2025 | 3.100 | Q3 |
JOURNAL OF MOLECULAR ENDOCRINOLOGY 最新收录文献
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1. On the biochemical assessment of maternal thyroid function and thyroid autoantibodies in pregnancy: a review.
PMID:日期:2026-09-23Thyroid disease is a common endocrine disorder in pregnant women and important to recognize. The clinical management relies on biochemical assessment of thyroid function and thyroid autoantibodies from a panel of routinely available tests. A challenge regarding biochemical assessment in pregnancy relates to the physiological adaptations that influence the analyses used for diagnosis and monitoring of maternal thyroid disease. The physiological adaptations include an increased activity of the thyroid gland, an increase in the levels of binding proteins, and a suppression of the immune system which implies that biochemical test results should be interpreted in the context of pregnancy. This narrative review will discuss the biochemical assessment of thyroid function and thyroid autoantibodies in pregnancy with a focus on the biochemical methods used and the interpretation of results including strategies for establishment of reference intervals. A key implication is that biochemical results obtained in pregnancy should be considered according to the timing of the blood sampling and the biochemical method used. This is reflected by recommendations on the use of method- and trimester-specific reference intervals as part of clinical care, but similar considerations apply when thyroid function tests and thyroid autoantibodies are evaluated as part of population monitoring and used for definition of exposure in scientific outcome studies. Future research is encouraged to support the biochemical assessment and interpretation of thyroid function tests and thyroid autoantibodies in pregnancy. Future perspectives include advancements in the biochemical methods and in the methodology applied for establishment of reference intervals or clinical decision limits.
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2. Proteome analysis of different tissues in pregnant women with gestational diabetes and type 1 diabetes mellitus.
PMID:日期:2026-09-16Gestational diabetes mellitus (GDM) and type 1 diabetes mellitus (T1DM) represent distinct hyperglycemic states during pregnancy. Although proteomic alterations have been described in plasma and placental tissues in GDM, no study has comprehensively compared proteomic changes across multiple relevant tissues in both GDM and T1DM within the same investigation. Tissue samples of omental adipose tissue (OAT), placental tissue (PT), and skeletal muscle tissue (SMT) from pregnant women with GDM and T1DM were obtained during cesarean delivery. Protein extracts were analyzed using two-dimensional gel electrophoresis and difference gel electrophoresis, followed by MALDI-TOF/TOF mass spectrometry for protein identification. Protein-protein interaction analysis was performed using STRING. Selected proteins were further examined by western blotting. We found that carbonic anhydrase 1 (CA1) emerged as the only protein consistently altered in all three tissues. CA1 was upregulated in OAT and PT in GDM but downregulated in the same tissues in T1DM; in SMT, it was downregulated in both groups. Alpha-enolase (ENOA) demonstrated a similar inverse pattern, being upregulated in PT and SMT in GDM but downregulated in T1DM. All of these changes identified by 2DE analysis were statistically significant (P < 0.05). The findings of this study demonstrated that CA1 expression was significantly upregulated in OAT and PT, and ENOA expression was upregulated in PT and SMT. These alterations may reflect differences in the metabolic and hyperglycemic environments of the two conditions and may represent candidate tissue-level markers. Further studies are required to determine their functional and clinical significance.
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3. A framework to map cAMP signalling nanodomains: phosphodiesterase-centred phosphoproteome-interactome networks (pPINs) in cardiac myocytes.
PMID:日期:2026-08-01Intracellular signalling is commonly represented as linear pathways that connect receptors to downstream effectors. While such models have been instrumental in defining signalling cascades, they fail to capture the spatial organisation that underlies signalling specificity in living cells. The cyclic adenosine monophosphate (cAMP) pathway provides a well-established example of this principle, where signalling is compartmentalised into nanometre-scale domains that generate highly localised and functionally distinct responses. However, a comprehensive framework for defining the molecular composition, spatial organisation and functional outputs of these signalling domains and how they adapt to perturbations remains lacking. Here, we discuss how integrative proteomics approaches can be used to reconstruct the subcellular cartography of compartmentalised signalling networks. By combining isoform-specific interactomics, quantitative phosphoproteomics, network analysis and spatial annotation, individual signalling platforms can be mapped within their native intracellular context. We introduce phosphoproteome-interactome networks (pPINs), a systems-level framework that integrates molecular interactions, subcellular localisation and phosphorylation responses to define phosphodiesterase (PDE)-centred signalling platforms and their associated signalling outputs. Using PDE3A isoforms as an example, we illustrate how pPINs uncover multiple spatially distinct cAMP signalling nanodomains in cardiac myocytes and reveal previously unrecognised biology, including a nuclear PDE3A2/SMAD4/HDAC-1 platform that locally constrains PKA activity and suppresses prohypertrophic gene expression. More broadly, pPINs provide a conceptual and computational framework for resolving the spatial architecture of intracellular signalling networks and establish a foundation for precision therapeutic strategies targeting discrete signalling microenvironments.
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4. An analysis of intestinal morphology and incretin-producing cells after sleeve gastrectomy in male mice.
PMID:日期:2026-08-01Sleeve gastrectomy (SG) is an effective treatment for obesity. SG increases glucagon-like peptide-1 (GLP-1) secretion; however, its effect on glucose-dependent insulinotropic polypeptide (GIP) remains unclear. Previous studies investigating changes in intestinal morphology, the number of GLP-1-producing cells (enteroendocrine L cells), and the number of GIP-producing cells (enteroendocrine K cells) after SG have been based on two-dimensional histological evaluations. In this study, we performed three-dimensional (3D) evaluations using a tissue-clearing method to precisely elucidate the intestinal morphology and incretin-producing cell number after SG in various tissue-specific reporter mouse strains. Insulin and GLP-1 secretion were significantly higher in SG mice compared with sham-operated mice, whereas GIP secretion did not differ between these two mouse groups. The villus length and width of the villus major axis in the duodenum were significantly shorter in SG mice. After SG, the number of villus L cells became significantly higher in the ileum, but did not change in the colon. After SG, the number of villus K cells became significantly lower in the duodenum. This is the first study to provide a 3D morphological evaluation of the entire intestine after SG. Intestinal morphology and the number and localization of incretin-producing cells within villi and crypts can be comprehensively quantified.
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5. Caspase-8 as a candidate mediator associated with everolimus resistance in neuroendocrine tumors.
PMID:日期:2026-08-01Everolimus, an mTORC1 inhibitor, is approved for treating pancreatic and lung neuroendocrine tumors (NETs), yet acquired resistance limits its long-term efficacy. The molecular mechanisms underlying resistance and potential strategies to overcome it remain poorly defined. RNA sequencing was performed in everolimus-sensitive and everolimus-resistant QGP-1 pancreatic NET cells (QS and QR, respectively) to identify transcriptional changes associated with everolimus resistance. Key differentially expressed genes were validated in QGP-1, H727 lung NET cells, and patient-derived Pa-NET cells using RT-qPCR. The potential functional involvement of caspase-8 (CASP8) was investigated pharmacologically using the preferential CASP8 inhibitor Z-IETD-FMK, alone or in combination with everolimus, by evaluating effects on cell viability and CASP activity. Differential expression analysis identified 292 genes significantly dysregulated in QR versus QS cells, including CASP8, A2M, MGP, PTGS1, and IGFBP5. Enrichment analysis highlighted pathways related to ECM remodeling, neuroactive ligand-receptor interactions, and GPCR signaling. Validation in H727 cells and primary Pa-NET samples showed some conserved transcriptional changes, with CASP8 upregulation emerging as a particularly consistent alteration. CASP8 inhibition reduced viability in both QS and QR cells, while combined Z-IETD-FMK and everolimus treatment produced the greatest decrease in QS viability and was associated with reduced CASP3/7 activity. Our study identifies CASP8 as a candidate mediator associated with everolimus resistance in NETs, together with alterations in ECM remodeling and receptor signaling. These findings support further investigation of CASP8-targeting strategies, particularly in combination with mTOR inhibition, as a potential approach to enhance therapeutic efficacy.
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6. BAMBI acts as a molecular switch to determine the cell fate of C2C12 myoblasts.
PMID:日期:2026-08-01Myogenesis is a tightly regulated process by a cascade of well-coordinated events and pathways. In addition to the known myogenic regulatory factor (MRF) family, including Myf5, MyoD, myogenin, and MRF4, our previous study identified that BAMBI is involved in muscle regeneration and siRNA-mediated BAMBI knockdown impairs C2C12 myoblast differentiation. However, the potential role of BAMBI in determining cell lineage and fate specification in C2C12 myoblasts remains unexplored. In this study, we analyzed the RNA-seq data and discovered that BAMBI expression was dynamically regulated during the proliferation and differentiation period of C2C12 myoblasts. By establishing a cell line with the loss of function and gain of function of BAMBI in C2C12 myoblasts, we demonstrated that BAMBI deletion totally abrogated myogenic differentiation of C2C12 myoblast cells. In addition, loss of BAMBI converts C2C12 myoblasts to brown adipocytes through downregulation of MyoD and upregulation of Prdm16. Conversely, BAMBI overexpression strikingly enhanced myogenic differentiation of C2C12 myoblasts by upregulating MyoD expression. Taken together, our results establish that BAMBI is a vital myogenic factor involved in myoblast differentiation and a key regulator governing the balance between myogenic and adipogenic lineages in C2C12 myoblast cells.
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7. Toxic crossroads: environmental pesticides and their endocrine footprints in global metabolic health.
PMID:日期:2026-08-01GRAPHICAL ABSTRACT Endocrine-disrupting pesticides (EDPs) exert deleterious effects on the endocrine system, with documented evidence implicating specific pesticides in endocrine disruption, resulting in developmental delays during puberty and thyroid gland dysfunction, thereby increasing susceptibility to metabolic diseases. The disruption of intracellular insulin signaling, which is characterized by redox imbalance, toxicological effects, and pro-inflammatory activity, facilitates cellular adaptation to stress. However, this adaptive response can aberrantly induce a dysfunctional feedback loop characterized by diminished cellular insulin responsiveness, a prevalent feature of metabolic disorders. Despite significant advancements in the scientific understanding of EDPs, substantial knowledge gaps and uncertainties persist, impeding progress toward improved health outcomes. This review highlights current findings on the metabolic toxicity of pesticides in the context of obesity and diabetes, concentrating on crucial signaling pathways and a mechanistic perspective that offers insight into resistance channels as reviewed. These findings enhance our understanding of the potential impacts of EDPs on human health.
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8. Chloride-permeable channels in white adipocytes: their role in adipogenesis and membrane potential.
PMID:日期:2026-08-01Ion fluxes, regulated by membrane potential (Vm), are vital to white fat adipocyte (WFA) function and adipogenesis. These processes present a novel target to intervene in obesity. To explore this possibility, we applied transcriptomics, immunohistochemistry, electrophysiology, and adipogenesis assays alongside siRNA and pharmacological tools to identify the chloride-permeable channel(s) that determine the Vm of WFA and to test whether those channels - specifically SWELL1 (Lrrc8 family), TTYH2/3, and EAAT1 - regulate adipocyte differentiation and adipogenesis. RNA sequencing and qPCR confirmed the existence of Lrrc8a, Lrrc8b, Lrrc8c, Lrrc8d, Ttyh2, Ttyh3, Slc1a1, and Ano1 transcripts across different primary fat depots of rats and mice, as well as a subset within 3T3-L1 adipocytes. The corresponding protein products, SWELL1 (Lrrc8x), TTYH2/3 (Ttyh2/3), and EAAT1 (Slc1a1), were found in both the plasma membrane and cytoplasm of primary and differentiated 3T3-L1 adipocytes, whereas TMEM16A protein was only in primary adipocytes and undifferentiated 3T3-L1 pre-adipocytes. Functional studies showed that although siRNA knockdown or pharmacological blockade of SWELL1, TTYH2/3, or EAAT1 proteins did not affect adipocyte Vm or electrophysiological characteristics, SWELL1 and TTYH2/3 knockdown significantly suppressed adipocyte differentiation and adipogenesis. Together, these findings reveal a role for SWELL1, TTYH2/3, and EAAT1 in adipogenesis and highlight their potential as targets for therapeutic strategies in obesity management. Although the precise chloride permeability responsible for adipocyte Vm remains to be defined, this work advances our understanding of adipocyte biology.
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9. A literature overview of age- and Tanner stage-specific reference intervals for sex hormones for children aged 0-18 years.
PMID:日期:2026-08-01This study aims to provide a comprehensive overview of age- and Tanner stage-specific reference intervals (RIs) for testosterone, estradiol, luteinizing hormone (LH), follicle-stimulating hormone (FSH), and sex hormone-binding globulin (SHBG) in children and adolescents and to highlight the importance of age- and Tanner stage-specific RIs for clinical practice. A literature review was performed to identify studies reporting RIs on testosterone and estradiol quantified using GC-MS/MS or LC-MS/MS and LH, FSH, and SHBG quantified using immunoassays in healthy individuals aged 0-18 years, categorized by age and/or Tanner stage. Sample sizes were evaluated according to the Clinical Laboratory Standards Institute (CLSI) guideline CLSI EP28-A3c, with ≥120 samples per group being acceptable, 39-119 samples being poor, and ≤38 samples being unacceptable. Analytical methods and statistical approaches were carefully documented. Fourteen studies were included for testosterone, seven for estradiol, thirteen for LH and FSH, and nine for SHBG. The results revealed considerable variability in the availability and quality of RIs, with many studies lacking adequate sample size or appropriate partitioning. Testosterone, estradiol, LH, and FSH RIs demonstrated significant changes during mini-puberty and puberty, with clear sex-specific patterns. SHBG RIs fluctuated throughout childhood and adolescence. This literature review demonstrates that RIs for HPG axis hormones show significant changes during mini-puberty and puberty, although data using appropriate analytical methods, using sufficient sample sizes, and reporting on age categories, Tanner stage, and menstrual cycle phase are scarce. Robust age- and Tanner stage-specific RIs are essential to improve diagnostic accuracy and individualized care in children and adolescents.
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10. Diabetes compromises DNA damage repair and telomere maintenance in adipose tissue stromal cells, leading to cellular senescence.
PMID:日期:2026-08-01Diabetes mellitus (DM) is characterized by chronic metabolic stress that promotes oxidative damage, genomic instability, and premature cellular ageing, with adipose tissue senescence being a pivotal contributor to metabolic dysfunction. Yet, the impact on DNA damage repair (DDR) and telomere maintenance in adipose tissue remains poorly defined. This study investigated DDR capacity, telomere integrity, and the senescence-associated secretory phenotype (SASP) in adipose tissue and adipose tissue-derived stromal cells (ADSCs) under diabetic conditions. Using an obese diabetic (ob/ob) mouse model, we confirmed whole-blood telomere shortening, significant adipose tissue hypertrophy, metabolic dysregulation, and elevated DNA damage, evidenced by increased γH2AX-positive staining. In vitro, ADSCs exposed to a diabetic microenvironment (AGEs and TNFα) exhibited increased reactive oxygen species and DNA damage without a corresponding activation of DDR pathways, as indicated by unchanged PARP1 levels and broad downregulation of key DNA repair genes, including sensors (ATM, ABL1, RAD17) and effectors across the MMR, NER, HR, and NHEJ pathways. This impaired genomic surveillance was accompanied by premature cellular senescence and a significant repression of genes involved in telomere protection (shelterin complex), telomerase activity, and telomere maintenance, together with marked telomere shortening following prolonged exposure. Furthermore, diabetic conditions increased the secretion of pro-inflammatory cytokines, chemokines, and growth factors. Collectively, these findings demonstrate that the diabetic microenvironment is associated with maladaptive DDR responses, telomere dysfunction, cellular senescence, and a pro-inflammatory secretory phenotype. This study highlights compromised genomic maintenance as a potential key mechanism underpinning adipose tissue dysfunction in DM and emphasizes the need for future investigations into the mechanisms underlying dysregulated DDR and telomere biology.