Evidence map›Paper›PMID 36595202›Full record

ReviewCurrent atherosclerosis reports2023

From 'Omics to Multi-omics Technologies: the Discovery of Novel Causal Mediators.

Pedrum Mohammadi-Shemirani, Tushar Sood, Guillaume Paré

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Current atherosclerosis reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
–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

35 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

3 authors.

Pedrum Mohammadi-Shemirani *Population Health Research Institute, David Braley Cardiac, Vascular and Stroke Research Institute, Hamilton, ON, Canada.
Tushar Sood *Temerty Faculty of Medicine, University of Toronto, Toronto, Canada.ORCID 0000-0002-4130-7100
Guillaume ParéPopulation Health Research Institute, David Braley Cardiac, Vascular and Stroke Research Institute, Hamilton, ON, Canada. pareg@mcmaster.ca.ORCID 0000-0002-6795-4760

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of review'Omics studies provide a comprehensive characterisation of a biological entity, such as the genome, epigenome, transcriptome, proteome, metabolome, or microbiome. This review covers the unique properties of these types of 'omics and their roles as causal mediators in cardiovascular disease. Moreover, applications and challenges of integrating multiple types of 'omics data to increase predictive power, improve causal inference, and elucidate biological mechanisms are discussed. RECENT

findingsMulti-omics approaches are growing in adoption as they provide orthogonal evidence and overcome the limitations of individual types of 'omics data. Studies with multiple types of 'omics data have improved the diagnosis and prediction of disease states and afforded a deeper understanding of underlying pathophysiological mechanisms, beyond any single type of 'omics data. For instance, disease-associated loci in the genome can be supplemented with other 'omics to prioritise causal genes and understand the function of non-coding variants. Alternatively, techniques, such as Mendelian randomisation, can leverage genetics to provide evidence supporting a causal role for disease-associated molecules, and elucidate their role in disease pathogenesis. As technologies improve, costs for 'omics studies will continue to fall and datasets will become increasingly accessible to researchers. The intrinsically unbiased nature of 'omics data is well-suited to exploratory analyses that discover causal mediators of disease, and multi-omics is an emerging discipline that leverages the strengths of each type of 'omics data to provide insights greater than the sum of its parts.

Indexed as

MultiomicsTranscriptomeHumansProteomeProteomeAtherosclerosisBiomarkersCardiovascular diseaseCausal inferenceMediatorsMulti-omics

Identifiers

PMID36595202
PMCPMC9807989

What Socratic holds

Textmetadata
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.