Evidence map›Paper›PMID 40185091›Full record

ReviewCell genomics2025

Variant-to-function approaches for adipose tissue: Insights into cardiometabolic disorders.

Sophia Metz, Jonathan Robert Belanich, Melina Claussnitzer, Tuomas Oskari Kilpeläinen

Abstract readReview
In one paragraph

Review in Cell genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Sophia MetzNovo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, 2200 Copenhagen, Denmark; The Novo Nordisk Foundation Center for Genomic Mechanisms of Disease, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Programs in Metabolism and Medical & Population Genetics, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Electronic address: sophia.metz@sund.ku.dk.
Jonathan Robert BelanichNovo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, 2200 Copenhagen, Denmark; The Novo Nordisk Foundation Center for Genomic Mechanisms of Disease, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Melina ClaussnitzerThe Novo Nordisk Foundation Center for Genomic Mechanisms of Disease, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Programs in Metabolism and Medical & Population Genetics, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Center for Genomic Medicine, Endocrine Division, Massachusetts General Hospital, Harvard Medical School, Cambridge, MA 02142, USA.
Tuomas Oskari KilpeläinenNovo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, 2200 Copenhagen, Denmark; The Novo Nordisk Foundation Center for Genomic Mechanisms of Disease, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Electronic address: tuomas.kilpelainen@sund.ku.dk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genome-wide association studies (GWASs) have identified thousands of genetic loci associated with cardiometabolic disorders. However, the functional interpretation of these loci remains a daunting challenge. This is particularly true for adipose tissue, a critical organ in systemic metabolism and the pathogenesis of various cardiometabolic diseases. We discuss how variant-to-function (V2F) approaches are used to elucidate the mechanisms by which GWAS loci increase the risk of cardiometabolic disorders by directly influencing adipose tissue. We outline GWAS traits most likely to harbor adipose-related variants and summarize tools to pinpoint the putative causal variants, genes, and cell types for the associated loci. We explain how large-scale perturbation experiments, coupled with imaging and multi-omics, can be used to screen variants' effects on cellular phenotypes and how these phenotypes can be tied to physiological mechanisms. Lastly, we discuss the challenges and opportunities that lie ahead for V2F research and propose a roadmap for future studies.

Indexed as

Adipose TissueCardiovascular DiseasesMetabolic DiseasesAnimalsGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansPhenotypeadipocyteadipogenesisadipose tissuebody fat distributioncardiometabolic diseasefunctional genomicsgenome editinggenome-wide association studynon-coding variantregulatory element

Identifiers

PMID40185091
PMCPMC12143332

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.