Nature Reviews Endocrinology自然综述：内分泌学
Nature Reviews Endocrinology(英文缩写 NAT REV ENDOCRINOL),ISSN 1759-5029,eISSN 1759-5037,中文译名:自然综述：内分泌学 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：2025-11-01 至 2026-10-31，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 | 47.564 | Q1 |
| 2022 | 40.500 | Q1 |
| 2023 | 31.000 | Q1 |
| 2024 | 40.000 | Q1 |
| 2025 | 39.100 | Q1 |
Nature Reviews Endocrinology 最新收录文献
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1. Diagnosis and management of Silver-Russell syndrome: second international consensus statement.
1. Silver-Russell综合征的诊断与管理：第二份国际共识声明PMID:日期:2026-09-23This international Consensus Statement updates 2016 guidelines for diagnosis and management of individuals with Silver-Russell syndrome (SRS), using a Delphi-like process to reach agreement through iterative expert discussions, based on published data and/or expert opinion. Individuals referred with suspected SRS show substantial clinical and genetic heterogeneity. Advances in genomic and epigenomic technology highlight the need for strict, primarily molecular, criteria for diagnosis, which should be made in those with maternal uniparental disomy for chromosome 7 (upd(7)mat) or 11p15 loss of methylation at H19/IGF2:intergenic differentially methylated region (IG-DMR) (due to an imprinting change, copy number variant or upd(11)mat). Molecular stratification enables tailoring of care pathways towards specific genetic and/or epigenetic subgroups. More widely, recommendations are relevant to other growth-related imprinting disorders (including Temple syndrome) and conditions affecting the insulin-like growth factor 2 pathway. An expert, multidisciplinary approach is required, focusing on growth failure, early severe feeding difficulties, later possible rapid weight gain, abnormal body composition, gastrointestinal problems, hypoglycaemia, insulin resistance, accelerated puberty, body asymmetry, neurocognitive issues and psychosocial challenges. Evidence published since the first Consensus Statement highlights the increased risk of metabolic disease from adolescence into adulthood. These updated recommendations have important implications for accurate diagnosis and optimal life-long management of individuals with SRS.
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2. The causes of cachexia: key signals and the brain.
2. 恶病质的成因：关键信号与大脑PMID:日期:2026-09-21Cachexia is a multisystem, complex disorder of body weight and body composition characterized by a relentless, non-resolving wasting of metabolic reserve that, although long recognized and described, continues to elude effective treatment. A continued focus on central nervous system pathways as key drivers of some of the cardinal features of cachexia now points towards the development of long-needed effective interventions. In this Review, we focus on several key signals, namely growth differentiation factor 15, melanocortins and interleukin-6, that illustrate the power of cross-disciplinary thinking to better understand how humoral signals affect body composition, behaviour and cognition in cachexia.
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3. Nutrition transitions, obesity and T2DM in the Middle East and North Africa.
PMID:日期:2026-09-18Obesity and type 2 diabetes mellitus (T2DM) are global epidemics, but their burden is particularly pronounced in the Middle East and North Africa (MENA) region. This Review provides a comprehensive overview of their epidemiological landscape among adults in the MENA region, encompassing disease burden, temporal trends, intersecting risk factors and key gaps in research, policy and practice, while highlighting regional heterogeneity. Despite worsening trends, the broader landscape, including disease burden and its drivers, remains insufficiently addressed. Contributing risk factors include poor diet quality, physical inactivity, genetic predisposition, obesogenic food environments and socioeconomic and cultural influences. While high-income places in the Gulf region have undergone earlier and more advanced nutrition transitions, with some of the highest prevalences of obesity and T2DM globally, places in North Africa are experiencing rapid shifts, with some of the steepest increases in high BMI and elevated fasting plasma levels of glucose. Although places share common drivers such as urbanization and sedentary lifestyles, the magnitude and distribution of risk vary widely owing to differences in economic development, healthcare infrastructure, cultural norms and public health nutrition policies. These epidemics impose a substantial and under-recognized economic burden. Prevention and management efforts remain fragmented, highlighting the need for stronger regional collaboration, improved evidence generation and culturally tailored interventions.
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6. High-fat diet promotes tumour formation in the epithelium.
6. 高脂饮食促进上皮肿瘤形成PMID:日期:2026-09-10该文献暂无摘要。
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7. Adjusting α-cell metabolism induces β-cell features.
7. 调整α细胞代谢可诱导β细胞特征PMID:日期:2026-09-07该文献暂无摘要。
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8. CheckCausesObesity.com: a screening and monitoring tool for obesity.
8. CheckCausesObesity.com：肥胖症的筛查和监测工具PMID:日期:2026-09-01该文献暂无摘要。
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10. Anaplastic thyroid cancer: genomic landscape, molecular drivers and novel therapeutics.
10. 未分化甲状腺癌：基因组景观、分子驱动因素和新型治疗PMID:日期:2026-08-25Anaplastic thyroid cancer (ATC) is one of the most aggressive human malignancies, defined by rapid progression, early metastasis and resistance to nearly all standard therapies. Although it accounts for less than 2% of thyroid cancers, ATC causes a disproportionate number of thyroid cancer-related deaths, with median overall survival rarely exceeding 10 months. Most patients present with unresectable or metastatic disease, leaving few curative options. The biology of ATC reflects a convergence of diverse oncogenic drivers and profound tumour plasticity. Frequent alterations in MAPK and PI3K pathways, loss of tumour suppressors and epigenetic deregulation fuel uncontrolled proliferation. A hypoxic and inflammatory microenvironment further promotes angiogenesis, immune evasion and metastatic spread. ATC cells also undergo extensive metabolic rewiring, shifting between glycolysis and oxidative phosphorylation to withstand nutrient and therapeutic stress. In parallel, stromal components, including fibroblasts, immune cells and endothelial networks, reinforce invasion and treatment resistance. In this Review, we highlight advances in the understanding of ATC biology, with a focus on driver genetic alterations, metabolic plasticity and microenvironmental interactions that underpin its exceptional aggressiveness. We also discuss how these biological insights provide a rationale for the design of multimodal therapeutic strategies urgently needed to improve outcomes for patients with ATC.