Evidence map›Paper›PMID 33513081›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2021

Characterization of βARKct engineered cellular extracellular vesicles and model specific cardioprotection.

Jin-Sook Kwon, Sarah M Schumacher, Erhe Gao, J Kurt Chuprun, Jessica Ibetti, Rajika Roy, Mohsin Khan, Raj Kishore, Walter J Koch

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 26% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Endogenous Engineering Reprograms Extracellular Vesicles for Enhanced Therapeutic Function.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Extracellular vesicle therapeutics for cardiac repair.Journal of molecular and cellular cardiology · 2025
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Extracellular vesicle-mediated bidirectional communication between heart and other organs.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  17. Review
  18. 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

9 authors at 1 institution in 1 country.

Jin-Sook KwonCenter for Translational Medicine, Department of Pharmacology, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania.
Sarah M SchumacherCenter for Translational Medicine, Department of Pharmacology, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania.ORCID 0000-0002-4941-7267
Erhe Gao
J Kurt ChuprunCenter for Translational Medicine, Department of Pharmacology, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania.
Jessica IbettiCenter for Translational Medicine, Department of Pharmacology, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania.
Rajika RoyCenter for Translational Medicine, Department of Pharmacology, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania.
Mohsin KhanCenter for Metabolic Disease Research, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania.ORCID 0000-0001-7007-1048
Raj KishoreCenter for Translational Medicine, Department of Pharmacology, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania.ORCID 0000-0002-8168-3004
Walter J KochCenter for Translational Medicine, Department of Pharmacology, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania.
Temple University · US

Funding

Regulation of Beta-Adrenergic Receptor Signaling by S-NitrosylationP01HL075443 · NHLBI · DUKE UNIVERSITY · PI STAMLER, JONATHAN S. · 2004 to 2019
$26.1M
Small and large animal surgery, physiology and histologyP01HL134608 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI Raj Kishore · 2017 to 2026
$21.0M
Targeting Pathways Involved in Cardiac Injury for Novel Repair StrategiesP01HL147841 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI KOCH, WALTER J. · 2020 to 2024
$11.4M
Targeting GRK2 in the HeartR01HL061690 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI KOCH, WALTER J. · 1998 to 2022
$4.2M
NHLBI NIH HHS P01 HL075443NHLBI NIH HHS P01 HL134608NHLBI NIH HHS P01 HL147841NHLBI NIH HHS R01 HL061690
6 · The paper itself

Abstract

Recent data supporting any benefit of stem cell therapy for ischemic heart disease have suggested paracrine-based mechanisms via extracellular vesicles (EVs) including exosomes. We have previously engineered cardiac-derived progenitor cells (CDCs) to express a peptide inhibitor, βARKct, of G protein-coupled receptor kinase 2, leading to improvements in cell proliferation, survival, and metabolism. In this study, we tested whether βARKct-CDC EVs would be efficacious when applied to stressed myocytes in vitro and in vivo. When isolated EVs from βARKct-CDCs and control GFP-CDCs were added to cardiomyocytes in culture, they both protected against hypoxia-induced apoptosis. We tested whether these EVs could protect the mouse heart in vivo, following exposure either to myocardial infarction (MI) or acute catecholamine toxicity. Both types of EVs significantly protected against ischemic injury and improved cardiac function after MI compared with mice treated with EVs from mouse embryonic fibroblasts; however, βARKct EVs treated mice did display some unique beneficial properties including significantly altered pro- and anti-inflammatory cytokines. Importantly, in a catecholamine toxicity model of heart failure (HF), myocardial injections of βARKct-containing EVs were superior at preventing HF compared with control EVs, and this catecholamine toxicity protection was recapitulated in vitro. Therefore, introduction of the βARKct into cellular EVs can have improved reparative properties in the heart especially against catecholamine damage, which is significant as sympathetic nervous system activity is increased in HF.

Indexed as

Stem Cell TransplantationAnimalsApoptosisCell HypoxiaCells, CulturedCytokinesDisease Models, AnimalExtracellular VesiclesG-Protein-Coupled Receptor Kinase 2Heart FailureInflammation MediatorsMaleMiceMice, Inbred C57BLMicroRNAsMyocardial Infarctionbeta-adrenergic receptor kinase inhibitory peptideCytokinesG-Protein-Coupled Receptor Kinase 2GRK2 protein, mouseInflammation MediatorsMicroRNAsPeptidesRecombinant Proteinscardiac derived cellscardiomyocytesextracellular vesiclesGRK2microRNAsβARKct

Identifiers

PMID33513081
PMCPMC8260382
OpenAlexW3121668128

What OpenQuestion 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 OpenQuestion graph.