Cell Metabolism
ISSN:1550-4131

Cell Metabolism

CELL METAB
学科领域:生物学
是否预警:不在预警名单内
是否OA:
录用周期:平均2.5月
新锐分区:生物学1区
年发文量:148
影响因子:30.9
JCR分区:Q1

基本信息

欢迎并感谢您考虑将您的工作提交给细胞代谢。2005年,细胞代谢是顶级研究期刊,致力于发表新颖的,有影响力的论文,涵盖基础到临床代谢研究。我们对研究生理稳态的分子机制以及疾病的问题感兴趣。该杂志的使命是为代谢界提供一个交流思想和概念的论坛,并促进跨学科研究和合作。为此,我们的目标是发表不仅在其领域内具有特殊意义的工作,而且对附近地区以外的研究人员也感兴趣的工作,以促进idea异花授粉。细胞代谢的范围包括糖尿病,肥胖,胰腺 β 细胞功能,脂肪组织生物学 (白色,棕色和米色),脂质代谢,心血管生物学,免疫代谢,骨稳态,衰老和应激反应,肌肉减少,中介代谢和癌症,恶病质,神经元控制代谢和引起神经变性的代谢紊乱,昼夜节律生物学,干细胞能量学,运动代谢,线粒体生物学和其他代谢细胞器,如过氧化物酶体和ER等。对于原创研究文章,可以使用不同的格式,例如 “研究文章”,“短文”,“临床和翻译报告” 和 “资源”。对于非研究 (前题) 文章,格式包括 “信函”,“论文”,“迷你评论”,“评论” 和 “透视”。
1550-4131SCIE/Scopus收录
30.9
34.8
2026年3月发布
点击查看历史分区趋势    >
大类学科小类学科Top期刊综述期刊
生物学1区
CELL BIOLOGY 细胞生物学
1区
ENDOCRINOLOGY & METABOLISM 内分泌学与代谢
1区
N/A
WOS期刊SCI分区  2024-2025最新升级版
按JIF指标学科分区收集子录JIF分区JIF排名百分位
学科:CELL BIOLOGY
SCIE
Q1
6/204
学科:ENDOCRINOLOGY & METABOLISM
SCIE
Q1
3/193
按JCR指标学科分区收集子录JCR分区JCR排名百分位
学科:CELL BIOLOGY
SCIE
Q1
5/204
学科:ENDOCRINOLOGY & METABOLISM
SCIE
Q1
2/193
219
148
7%约12.5%平均2.5月-生物-内分泌学与代谢
1.6%
时间预警情况
2026年03月发布的新锐学术版不在预警名单中
2025年03月发布的2025版不在预警名单中
2024年02月发布的2024版不在预警名单中
2023年01月发布的2023版不在预警名单中
2021年12月发布的2021版不在预警名单中
2020年12月发布的2020版不在预警名单中
79.73%22.69%7.01%
CiteScore:45.50
SJR:11.989
SNIP:4.912
学科类别分区排名百分位
大类:Biochemistry, Genetics and Molecular Biology
小类:Physiology
Q1
2 / 190
大类:Biochemistry, Genetics and Molecular Biology
小类:Cell Biology
Q1
3 / 285
大类:Biochemistry, Genetics and Molecular Biology
小类:Molecular Biology
Q1
6 / 410

期刊高被引文献

Caloric Restriction Mimetics against Age-Associated Disease: Targets, Mechanisms, and Therapeutic Potential.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.01.018
GDF15 Provides an Endocrine Signal of Nutritional Stress in Mice and Humans
来源期刊:Cell MetabolismDOI:10.1016/j.cmet.2018.12.016
Exercise-Induced Changes in Visceral Adipose Tissue Mass Are Regulated by IL-6 Signaling: A Randomized Controlled Trial.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2018.12.007
The Mouse Microbiome Is Required for Sex-Specific Diurnal Rhythms of Gene Expression and Metabolism
来源期刊:Cell MetabolismDOI:10.1016/j.cmet.2018.09.023
Lymphocyte-Derived Exosomal MicroRNAs Promote Pancreatic β Cell Death and May Contribute to Type 1 Diabetes Development.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2018.09.011
Extracellular Vesicle-Contained eNAMPT Delays Aging and Extends Lifespan in Mice.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.05.015
Cholesterol Induces CD8+ T Cell Exhaustion in the Tumor Microenvironment.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.04.002
NAD+ in Brain Aging and Neurodegenerative Disorders.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.09.001
Genetic Analysis Reveals AMPK Is Required to Support Tumor Growth in Murine Kras-Dependent Lung Cancer Models.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2018.10.005
A Map of Human Type 1 Diabetes Progression by Imaging Mass Cytometry.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2018.11.014
Choline Uptake and Metabolism Modulate Macrophage IL-1β and IL-18 Production.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.03.011
Preserving Insulin Secretion in Diabetes by Inhibiting VDAC1 Overexpression and Surface Translocation in β Cells
来源期刊:Cell MetabolismDOI:10.1016/j.cmet.2018.09.008
Mitochondrial Damage and Activation of the STING Pathway Lead to Renal Inflammation and Fibrosis.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.08.003
Mediation of the Acute Stress Response by the Skeleton.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.08.012
Lactate Buildup at the Site of Chronic Inflammation Promotes Disease by Inducing CD4+ T Cell Metabolic Rewiring
来源期刊:Cell MetabolismDOI:10.1016/j.cmet.2019.10.004
Non-Canonical Control of Neuronal Energy Status by the Na+ Pump.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2018.11.005
Epithelial-Mesenchymal Transition Directs Stem Cell Polarity via Regulation of Mitofusin.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2018.11.004
Cell Clustering Promotes a Metabolic Switch that Supports Metastatic Colonization
来源期刊:Cell MetabolismDOI:10.1016/j.cmet.2019.07.014
Acyl-CoA-Binding Protein Drives Glioblastoma Tumorigenesis by Sustaining Fatty Acid Oxidation.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.04.004
Deubiquitinases Maintain Protein Homeostasis and Survival of Cancer Cells upon Glutathione Depletion.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.01.020
Microbial Metabolite Signaling Is Required for Systemic Iron Homeostasis.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.10.005
Acyl-CoA-Binding Protein Is a Lipogenic Factor that Triggers Food Intake and Obesity.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.07.010
Neurocognitive and Hormonal Correlates of Voluntary Weight Loss in Humans.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2018.09.024
Calcium Signaling Controls Pathogenic Th17 Cell-Mediated Inflammation by Regulating Mitochondrial Function.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.01.019
Transient Receptor Potential V Channels Are Essential for Glucose Sensing by Aldolase and AMPK
来源期刊:Cell MetabolismDOI:10.1016/j.cmet.2019.05.018
Aerobic Plus Resistance Exercise in Obese Older Adults Improves Muscle Protein Synthesis and Preserves Myocellular Quality Despite Weight Loss.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.06.008
Revisiting How the Brain Senses Glucose-And Why.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2018.11.001
Targeting Peripheral CB1 Receptors Reduces Ethanol Intake via a Gut-Brain Axis.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.04.012
Gut-Proglucagon-Derived Peptides Are Essential for Regulating Glucose Homeostasis in Mice.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.08.009
Tanycytes Regulate Lipid Homeostasis by Sensing Free Fatty Acids and Signaling to Key Hypothalamic Neuronal Populations via FGF21 Secretion.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.08.004
Acylglycerol Kinase Maintains Metabolic State and Immune Responses of CD8+ T Cells.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.05.016
Fructose-1,6-Bisphosphatase 2 Inhibits Sarcoma Progression by Restraining Mitochondrial Biogenesis.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.10.012
Patient-Driven Diabetes Care of the Future in the Technology Era.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2018.09.005
The DAPA-HF Trial: A Momentous Victory in the War against Heart Failure.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.10.008
AMPK-Mediated Lysosome Biogenesis in Lung Cancer Growth.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2018.12.011
United They Stand, Divided They Fall.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.09.008
Disruption of Acetyl-Lysine Turnover in Muscle Mitochondria Promotes Insulin Resistance and Redox Stress without Overt Respiratory Dysfunction.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.11.003
The Untapped Opportunity and Challenge of Immunometabolism: A New Paradigm for Drug Discovery.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.11.014
Insulin-Driven PI3K-AKT Signaling in the Hepatocyte Is Mediated by Redundant PI3Kα and PI3Kβ Activities and Is Promoted by RAS.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.03.010
Regulatory T Cells under the Mercy of Mitochondria.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.01.012
Host Control of Tumor Feeding: Autophagy Holds the Key.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.01.009
Adipose Tissue B Cells Come of Age: The AABs of Fat Inflammation.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.11.007
New Insights into the Regulation of Leptin Gene Expression.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.04.005
A Gut Check Explains Improved Glucose Metabolism after Surgery.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.10.002
Gut T Cells Feast on GLP-1 to Modulate Cardiometabolic Disease.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.03.002
Metabolic Adaptation Fuels Lymph Node Metastasis.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.03.006
Mitochondrial DNA Inheritance in Humans: Mix, Match, and Survival of the Fittest.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.07.009
Acyl-CoA-Binding Protein Fuels Gliomagenesis.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.07.007
The Transsulfuration Pathway Makes, the Tumor Takes.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.10.009
TMEM2 Modulates ER Stress in a Non-canonical Manner.
来源期刊:Cell metabolismDOI:10.1016/j.cmet.2019.11.008

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