Evidence map›Paper›PMID 39234691›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2024

Spatial Transcriptomic Approach to Understanding Coronary Atherosclerotic Plaque Stability.

Maria G Gastanadui, Camilla Margaroli, Silvio Litovsky, Robert P Richter, Dezhi Wang, Dongqi Xing, J Michael Wells, Amit Gaggar, Vivek Nanda, Rakesh P Patel and 1 more

Abstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing 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

42 citing papers in PubMed.

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  17. More Than a Cleanup Crew: The Expanding Biology of Efferocytosis.Arteriosclerosis, thrombosis, and vascular biology · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Maria G GastanaduiDepartment of Medicine, Division of Cardiovascular Disease (M.G.G., G.A.P.), University of Alabama at Birmingham.
Camilla MargaroliDepartment of Pathology, Division of Molecular and Cellular Pathology (C.M., V.N., R.P.P.), University of Alabama at Birmingham.ORCID 0000-0003-3952-0778
Silvio LitovskyDepartment of Pathology, Division of Anatomic Pathology (S.L.), University of Alabama at Birmingham.ORCID 0000-0002-3174-2192
Robert P RichterProgram in Protease/Matrix Biology (C.M., R.P.R., D.X., J.M.W., A.G., R.P.P., G.A.P.), University of Alabama at Birmingham.ORCID 0000-0002-3753-1994
Dezhi WangDepartment of Pathology, Pathology Core Research Laboratory (D.W.), University of Alabama at Birmingham.ORCID 0000-0002-6265-9607
Dongqi XingCardiopulmonary Research Program, Department of Medicine (M.G.G., D.X., J.M.W., A.G., R.P.P., G.A.P.), University of Alabama at Birmingham.ORCID 0000-0003-2227-3571
J Michael WellsCardiopulmonary Research Program, Department of Medicine (M.G.G., D.X., J.M.W., A.G., R.P.P., G.A.P.), University of Alabama at Birmingham.ORCID 0000-0001-9612-5454
Amit GaggarCardiopulmonary Research Program, Department of Medicine (M.G.G., D.X., J.M.W., A.G., R.P.P., G.A.P.), University of Alabama at Birmingham.ORCID 0000-0003-1586-5632
Vivek NandaDepartment of Pathology, Division of Molecular and Cellular Pathology (C.M., V.N., R.P.P.), University of Alabama at Birmingham.ORCID 0000-0003-1724-7168
Rakesh P PatelCardiopulmonary Research Program, Department of Medicine (M.G.G., D.X., J.M.W., A.G., R.P.P., G.A.P.), University of Alabama at Birmingham.ORCID 0000-0002-1526-4303
Gregory A PayneDepartment of Medicine, Division of Cardiovascular Disease (M.G.G., G.A.P.), University of Alabama at Birmingham.ORCID 0000-0002-8525-8603

Funding

A Novel Exosomal Inflammatory PathwayR35HL135710 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BLALOCK, J EDWIN · 2017 to 2023
$6.8M
Matrikines and COPD-PHR01HL148215 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI WELLS, JAMES MICHAEL · 2019 to 2023
$2.4M
Mechanisms driving endothelial angiopoietin-2 expression and vascular dysfunction during pediatric sepsisK08GM144788 · NIGMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI RICHTER, ROBERT P · 2021 to 2025
$930k
Extracellular matrix-derived chemokines mediate smoking-associated coronary atherosclerosisI01CX002495 · VA · BIRMINGHAM VA MEDICAL CENTER · PI Gregory Allen Payne · 2024 to 2026
–
CSRD VA I01 CX002495NHLBI NIH HHS R01 HL148215NHLBI NIH HHS R35 HL135710NIGMS NIH HHS K08 GM144788
6 · The paper itself

Abstract

backgroundCoronary atherosclerotic plaques susceptible to acute coronary syndrome have traditionally been characterized by their surrounding cellular architecture. However, with the advent of intravascular imaging, novel mechanisms of coronary thrombosis have emerged, challenging our contemporary understanding of acute coronary syndrome. These intriguing findings underscore the necessity for a precise molecular definition of plaque stability. Considering this, our study aimed to investigate the vascular microenvironment in patients with stable and unstable plaques using spatial transcriptomics.

methodsAutopsy-derived coronary arteries were preserved and categorized by plaque stability (n=5 patients per group). We utilized the GeoMx spatial profiling platform and Whole Transcriptome Atlas to link crucial histological morphology markers in coronary lesions with differential gene expression in specific regions of interest, thereby mapping the vascular transcriptome. This innovative approach allowed us to conduct cell morphological and spatially resolved transcriptional profiling of atherosclerotic plaques while preserving crucial intercellular signaling.

resultsWe observed intriguing spatial and cell-specific transcriptional patterns in stable and unstable atherosclerotic plaques, showcasing regional variations within the intima and media. These regions exhibited differential expression of proinflammatory molecules (eg, IFN-γ [interferon-γ], MHC [major histocompatibility complex] class II, proinflammatory cytokines) and prothrombotic signaling pathways. By using lineage tracing through spatial deconvolution of intimal CD68

conclusionsOur study illuminates distinct cell-specific and regional transcriptional alterations present in unstable plaques. Furthermore, we characterize spatially resolved, in situ evidence supporting cellular transdifferentiation and intraplaque plasticity as significant contributors to plaque instability in human coronary atherosclerosis. Our results provide a powerful resource for the identification of novel mediators of acute coronary syndrome, opening new avenues for preventative and therapeutic treatments.

Indexed as

Coronary Artery DiseaseCoronary VesselsGene Expression ProfilingPlaque, AtheroscleroticTranscriptomeAgedAutopsyCellular MicroenvironmentFemaleHumansMaleMiddle AgedRupture, Spontaneousacute coronary syndromeatherosclerosiscoronary thrombosismacrophagesmuscle, smooth, vascular

Identifiers

PMID39234691
PMCPMC11499036

What Socratic holds

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Registered trials

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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.