技能 细胞代谢期刊投稿要求指南

细胞代谢期刊投稿要求指南

v20260724
cell-metabolism
本技能为作者提供投稿给《细胞代谢》期刊的全面指南。它详细阐述了期刊的领域定位、研究范围,并强调了对体内生理学证据和机制深度的极高要求(如代谢物追踪、基因作图)。帮助作者预先评估稿件是否达到了该领域的顶尖科学标准。
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概览

Cell Metabolism (cell-metabolism)

Journal positioning

Cell Metabolism is Cell Press's flagship metabolism and physiology journal, publishing mechanistic studies of how organisms sense, process, and adapt to nutrients, energy, and metabolic stress — with emphasis on in vivo physiology and disease relevance. The core territory is metabolic disease (obesity, type 2 diabetes, NAFLD/NASH, cardiovascular-metabolic risk), mitochondrial biology, aging and longevity, and the metabolic underpinning of organ crosstalk. The readership spans metabolic biologists, physiologists, endocrinologists, and disease-oriented researchers; papers must deliver a mechanistic advance with in vivo grounding, not just a cell-culture phenotype.

This skill is a fit / venue-selection / re-framing tool. It does not replace the journal's current official submission guidelines. Before submitting, re-check the live author instructions on the Cell Press site or submission system.

When to trigger

  • The author names Cell Metabolism as the target venue.
  • A metabolism/physiology study is deciding between Cell Metabolism and Nature Metabolism, Cell, or a society metabolism journal.
  • An in vivo metabolic study needs to assess whether its mechanistic depth and disease relevance meet the bar.
  • The author needs this venue's desk-reject patterns and re-routing options.

Scope & topic fit

  • Energy homeostasis mechanisms: nutrient sensing (mTOR, AMPK, insulin signaling), fuel switching, and systemic energy balance studied in vivo.
  • Adipose biology, hepatic metabolism, skeletal-muscle fuel utilization — when the mechanistic insight is physiologically grounded.
  • Mitochondrial function and dysfunction in physiology and disease: electron transport, dynamics, mitophagy, inter-organellar communication.
  • Metabolic aging and longevity mechanisms: calorie restriction mimetics, mTOR/IGF-1/NAD pathways, senescence-metabolism interactions.
  • Gut-microbiome interactions with host metabolism when the host-side mechanism is the primary advance.
  • Immuno-metabolism and cancer metabolism are in scope when the metabolic mechanism — not the immune or cancer phenotype — is the central contribution.

Method & evidence bar

  • In vivo physiology is the default expectation: genetic mouse models (whole-body or tissue-specific knockouts, knock-ins), dietary or pharmacological perturbation with careful phenotyping (indirect calorimetry, glucose and insulin tolerance, clamp studies, metabolic cage data).
  • Mechanism must go beyond phenotype: genetic epistasis, metabolite tracing (stable isotope / 13C flux), or biochemical pathway validation is expected.
  • Metabolite profiling or metabolomics should be hypothesis-driven and mechanistically interpreted; untargeted discovery alone is insufficient.
  • Translation to human tissue (biopsies, organoids, or cohort correlations) is valued but not always mandatory; absence must be justified.
  • STAR Methods required; reagent/data deposition (metabolomics to MetaboLights or equivalent, sequencing to GEO, animal model details) per Cell Press policy.
  • Rigor reporting: blinding of outcome assessment in animal studies, group sizes with power justification, sex as a biological variable addressed.

Structure & house style

  • STAR Methods is mandatory; key resources table covers antibodies, mouse strains, software, metabolites/reagents.
  • Structured abstract with an "in brief" or "highlights" box; the title is declarative and states the physiological mechanism or disease connection.
  • Figures should build a coherent physiological narrative: establish the in vivo phenotype, determine the tissue/cell of action, identify the molecular mechanism, confirm with epistasis or rescue.
  • Graphical abstract standard for Cell Press; source data for all quantitative figures required.
  • Translational framing in the introduction and discussion must be specific: name the disease context, not just "metabolic syndrome."
  • Data and code availability statement required; statistical methods including treatment of sex and replication must be explicit.

Official-submission checklist

  • Before giving submission-ready advice, read ../../resources/source-basis.md and ../../resources/official-source-map.md; start from the official source anchors for this journal family, then cite the current journal-specific page you checked.
  • Search "Cell Metabolism author information" on the Cell Press site and follow the current version.
  • Re-check article types (Article, Short Article, Resource), length and figure limits, and supplemental policy.
  • Confirm STAR Methods and key resources table requirements for the current submission cycle.
  • Re-check animal ethics approval, sex-as-biological-variable reporting, and ARRIVE guidelines compliance.
  • Verify competing-interests, funding, and AI-use disclosure requirements.
  • Re-check data/metabolomics/sequencing deposition requirements and open-access/license options.
  • If the live official instructions conflict with this skill, the official instructions win.

Pre-submission self-check

  • One sentence stating the physiological mechanism discovered and its relevance to a metabolic disease or aging.
  • The advance is framed as a mechanistic insight, not as "gene X affects body weight."
  • In vivo data are central; if cell culture predominates, the physiological relevance is rigorously established.
  • Sex as a biological variable is explicitly addressed in the experimental design and statistics.
  • STAR Methods, key resources table, and data/code deposition are prepared.
  • Metabolite tracing, genetic epistasis, or equivalent mechanistic evidence supports causal conclusions.

Common desk-reject triggers

  • Entirely cell-based study with no in vivo component and no convincing justification for why in vivo work is impossible.
  • Phenotypic description in a knockout mouse without a mechanistic explanation of how the target drives the metabolic phenotype.
  • Metabolomics or proteomics survey with no mechanistic follow-through — a correlation list, not an advance.
  • Sex as a biological variable ignored in animal studies without justification.
  • Clinical or epidemiological study without a mechanistic molecular story — better suited to Diabetes Care, Cell Reports Medicine, or a clinical endocrinology journal.

Re-routing decision

  • Paradigm-shifting metabolic advance with extremely broad significance → cell (if the conceptual reach spans beyond metabolism) or nature / science.
  • Strong metabolic mechanism but somewhat narrower scope → nature-metabolism (Springer Nature; same tier, slightly broader tolerance for translational-only studies).
  • Cancer-metabolic mechanism with cancer biology as the primary frame → cancer-cell or molecular-cell.
  • Solid mechanistic work below the Cell Metabolism significance bar → elife, plos-biology, or a society journal such as Diabetes or the Journal of Lipid Research.

Output format

[Fit] High / Medium / Low (one-line reason)
[Target] Cell Metabolism
[Topic tags] <2–3 closest topics>
[Method/evidence] <does the in vivo physiology + mechanism clear Cell Metabolism's bar?>
[Top risk] <the single most likely reason for rejection>
[Official items to re-check] <article type/length / STAR Methods / animal ethics / sex-as-variable / data-code deposition>
[Re-route suggestion] <if not a fit, a better-matched venue>
信息
Category 未分类
Name cell-metabolism
版本 v20260724
大小 7.55KB
更新时间 2026-07-28
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