Evidence map›Paper›PMID 36459456›Full record

ArticleClinical science (London, England : 1979)2022

Translating atherosclerosis research from bench to bedside: navigating the barriers for effective preclinical drug discovery.

Lauren T May, Belinda A Bartolo, David G Harrison, Tomasz Guzik, Grant R Drummond, Gemma A Figtree, Rebecca H Ritchie, Kerry-Anne Rye, Judy B de Haan

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical science (London, England : 1979), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 20% of its field
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

13 citing papers in PubMed, 17 citations in OpenAlex.

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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

9 authors at 7 institutions in 4 countries.

Lauren T May *Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Victoria 3052, Australia.
Belinda A Bartolo *Faculty of Medicine and Health, University of Sydney, Sydney, Australia.
David G HarrisonDivision of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville TN, U.S.A.
Tomasz GuzikInstitute of Cardiovascular and Medical Sciences, University of Glasgow, U.K.
Grant R DrummondCentre for Cardiovascular Biology and Disease Research, Department of Microbiology, Anatomy, Physiology and Pharmacology, La Trobe University, Melbourne, Victoria, Australia.
Gemma A FigtreeKolling Research Institute, University of Sydney, Sydney, Australia.
Rebecca H RitchieDrug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Victoria, Australia.ORCID 0000-0002-8610-0058
Kerry-Anne RyeLipid Research Group, School of Medical Sciences, Faculty of Medicine, University of New South Wales, Sydney 2052, Australia.
Judy B de HaanCardiovascular Inflammation and Redox Biology Lab, Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia.
Monash University · AUThe University of Sydney · AUBaker Heart and Diabetes Institute · AUJagiellonian University · PLLa Trobe University · AUUNSW Sydney · AUVanderbilt University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular disease (CVD) remains the leading cause of death worldwide. An ongoing challenge remains the development of novel pharmacotherapies to treat CVD, particularly atherosclerosis. Effective mechanism-informed development and translation of new drugs requires a deep understanding of the known and currently unknown biological mechanisms underpinning atherosclerosis, accompanied by optimization of traditional drug discovery approaches. Current animal models do not precisely recapitulate the pathobiology underpinning human CVD. Accordingly, a fundamental limitation in early-stage drug discovery has been the lack of consensus regarding an appropriate experimental in vivo model that can mimic human atherosclerosis. However, when coupled with a clear understanding of the specific advantages and limitations of the model employed, preclinical animal models remain a crucial component for evaluating pharmacological interventions. Within this perspective, we will provide an overview of the mechanisms and modalities of atherosclerotic drugs, including those in the preclinical and early clinical development stage. Additionally, we highlight recent preclinical models that have improved our understanding of atherosclerosis and associated clinical consequences and propose model adaptations to facilitate the development of new and effective treatments.

Indexed as

AtherosclerosisCardiovascular DiseasesAnimalsDrug DiscoveryHumansModels, Animalatherosclerosiscardiovascular diseasecoronary artery diseasedrug discovery and designmodel organisms

Identifiers

PMID36459456
PMCPMC9727216
OpenAlexW4311125931

What Socratic holds

Textmetadata
LicenceCC BY
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.