Agent Skills
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cell-metabolism
GitHub用于评估代谢与生理学稿件是否适合Cell Metabolism期刊。提供选题匹配、机制深度与体内实验标准、拒稿模式及改投建议，辅助作者判断稿件契合度并优化投稿策略。
Trigger Scenarios
作者指定Cell Metabolism为目标期刊
在Cell Metabolism与其他代谢类期刊间犹豫
评估体内代谢研究的机制深度与疾病相关性
了解该刊拒稿规律及改投建议
Install
npx skills add brycewang-stanford/Awesome-Journal-Skills --skill cell-metabolism -g -y
SKILL.md
Frontmatter
{
"name": "cell-metabolism",
"description": "Use when targeting Cell Metabolism or deciding whether a metabolism\/physiology manuscript fits this venue. Encodes the journal's fit, framing, method-and-evidence bar, house style, official-submission re-check, and desk-reject heuristics."
}
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.mdand../../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) ornature/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-cellormolecular-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>
Version History
- 1839142 Current 2026-07-05 12:59
