Evidence map›Paper›PMID 38693202›Full record

ArticleScientific reports2024

Transcriptome analysis of cardiac endothelial cells after myocardial infarction reveals temporal changes and long-term deficits.

Chitra Basu, Presley L Cannon, Cassandra P Awgulewitsch, Cristi L Galindo, Eric R Gamazon, Antonis K Hatzopoulos

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Molecular Mechanisms Governing Vascular Function in Heart Failure.Arteriosclerosis, thrombosis, and vascular biology · 2026
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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

6 authors at 2 institutions in 1 country.

Chitra BasuDivision of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Presley L CannonDivision of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Cassandra P AwgulewitschDivision of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Cristi L GalindoDivision of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Eric R GamazonDivision of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Antonis K HatzopoulosDivision of Cardiovascular Medicine, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA. antonis.hatzopoulos@vumc.org.ORCID http://orcid.org/0000-0001-5610-0017
Vanderbilt University Medical Center · USUniversity of Pittsburgh · US

Funding

Training In Cardiovascular ResearchT32HL007411 · NHLBI · VANDERBILT UNIVERSITY · PI BECKMAN, JOSHUA A · 1985 to 2020
$7.2M
Functional heterogeneity of cardiac reparative cells after injuryR01HL138519 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HATZOPOULOS, ANTONIS · 2017 to 2020
$1.6M
Advancing Multi-Omics and Electronic Health Records Computational MethodologiesR01HG011138 · NHGRI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI GAMAZON, ERIC R · 2020 to 2024
$1.6M
Advancing drug repositioning and development for Alzheimer's Disease using functional genomics and computational phenomicsR56AG068026 · NIA · VANDERBILT UNIVERSITY MEDICAL CENTER · PI GAMAZON, ERIC R · 2021 to 2022
$1.5M
The anti-fibrotic effects of neuregulin in the heartK01HL121045 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI GALINDO, CRISTI LARA · 2014 to 2018
$747k
NHGRI NIH HHS R01 HG011138NHLBI NIH HHS K01 HL121045NHLBI NIH HHS R01 HL138519NHLBI NIH HHS T32 HL007411NIA NIH HHS R56 AG068026NIH HHS HL007411NIH HHS K01HL121045NIH HHS R01HG011138NIH HHS R01HL138519
6 · The paper itself

Abstract

Endothelial cells (ECs) have essential roles in cardiac tissue repair after myocardial infarction (MI). To establish stage-specific and long-term effects of the ischemic injury on cardiac ECs, we analyzed their transcriptome at landmark time points after MI in mice. We found that early EC response at Day 2 post-MI centered on metabolic changes, acquisition of proinflammatory phenotypes, initiation of the S phase of cell cycle, and activation of stress-response pathways, followed by progression to mitosis (M/G2 phase) and acquisition of proangiogenic and mesenchymal properties during scar formation at Day 7. In contrast, genes involved in vascular physiology and maintenance of vascular tone were suppressed. Importantly, ECs did not return to pre-injury phenotypes after repair has been completed but maintained inflammatory, fibrotic and thrombotic characteristics and lost circadian rhythmicity. We discovered that the highest induced transcript is the mammalian-specific Sh2d5 gene that promoted migration and invasion of ECs through Rac1 GTPase. Our results revealed a synchronized, temporal activation of disease phenotypes, metabolic pathways, and proliferation in quiescent ECs after MI, indicating that precisely-timed interventions are necessary to optimize cardiac tissue repair and improve outcomes. Furthermore, long-term effects of acute ischemic injury on ECs may contribute to vascular dysfunction and development of heart failure.

Indexed as

Endothelial CellsGene Expression ProfilingMyocardial InfarctionAnimalsCell MovementCell ProliferationDisease Models, AnimalMaleMiceMice, Inbred C57BLMyocardiumrac1 GTP-Binding ProteinTranscriptomerac1 GTP-Binding Protein

Identifiers

PMID38693202
PMCPMC11063162
OpenAlexW4396546180

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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 OpenQuestion graph.