ArticleCirculation2013
Age-associated defects in EphA2 signaling impair the migration of human cardiac progenitor cells.
Article in Circulation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 21 papers.
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.
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.
Who cites it
21 citing papers in PubMed, 39 citations in OpenAlex.
- Stimulatory Effects of Mesenchymal Stem Cells on cKit+ Cardiac Stem Cells Are Mediated by SDF1/CXCR4 and SCF/cKit Signaling Pathways.Circulation research · 2016Trial
- Structural and non-structural proteins in SARS-CoV-2: potential aspects to COVID-19 treatment or prevention of progression of related diseases.Cell communication and signaling : CCS · 2023Review
- Roles of Eph-Ephrin Signaling in the Eye Lens Cataractogenesis, Biomechanics, and Homeostasis.Frontiers in cell and developmental biology · 2022Review
- Single-Cell Transcriptomics of Human Mesenchymal Stem Cells Reveal Age-Related Cellular Subpopulation Depletion and Impaired Regenerative Function.Stem cells (Dayton, Ohio) · 2019Article
- Assessing Stem Cell DNA Integrity for Cardiac Cell Therapy.Journal of visualized experiments : JoVE · 2019Article
- Biology of Tendon Stem Cells and Tendon in Aging.Frontiers in genetics · 2019Review
- Decline in cellular function of aged mouse c-kitThe Journal of physiology · 2017Article
- p53 Modulates the Fate of Cardiac Progenitor Cells Ex Vivo and in the Diabetic Heart In Vivo.EBioMedicine · 2017Article
- Combined Analysis of Endothelial, Hematopoietic, and Mesenchymal Stem Cell Compartments Shows Simultaneous but Independent Effects of Age and Heart Disease.Stem cells international · 2017Article
- Remodeling the Human Adult Stem Cell Niche for Regenerative Medicine Applications.Stem cells international · 2017Review
- Current Understanding of the Pathways Involved in Adult Stem and Progenitor Cell Migration for Tissue Homeostasis and Repair.Stem cell reviews and reports · 2016Review
- miR-204 downregulates EphB2 in aging mouse hippocampal neurons.Aging cell · 2016Article
- Accumulation of Mitochondrial DNA Mutations Disrupts Cardiac Progenitor Cell Function and Reduces Survival.The Journal of biological chemistry · 2015Article
- Cardiac aging - Getting to the stem of the problem.Journal of molecular and cellular cardiology · 2015Review
- Rejuvenating the senescent heart.Current opinion in cardiology · 2015Review
- Eph receptors and ephrins: therapeutic opportunities.Annual review of pharmacology and toxicology · 2015Review
- Activation of EphA4 and EphB2 Reverse Signaling Restores the Age-Associated Reduction of Self-Renewal, Migration, and Actin Turnover in Human Tendon Stem/Progenitor Cells.Frontiers in aging neuroscience · 2015Article
- Aging disrupts cell subpopulation dynamics and diminishes the function of mesenchymal stem cells.Scientific reports · 2014Article
- Cardiac stem cells: biology and clinical applications.Antioxidants & redox signaling · 2014Review
- Predicting the future with stem cells.Circulation · 2014Article
Corrections and comments
- Retraction · 2018-12-12Concerns/Issues about Data · Investigation by Company/Institution · Misconduct - Official Investigation(s) and/or Finding(s) · Upgrade/Update of Prior Notice(s) · · Article corrected earlier; P Anversa named for conflict disclosure;
- Expression of concern · 2018-11-20Concerns/Issues about Data · Investigation by Company/Institution · Misconduct - Official Investigation(s) and/or Finding(s) · Updated to Retraction · Upgrade/Update of Prior Notice(s) · · Article corrected earlier; P Anversa named for conflict disclosure;
- Correction · 2015-12-01Conflict of Interest · Investigation by Company/Institution · Legal Reasons and/or Threats · Objections by Author(s) · Upgrade/Update of Prior Notice(s) · · Article corrected earlier; P Anversa named for conflict disclosure;
- Correction · 2015-07-28Concerns/Issues about Data · Concerns/Issues about Image · Investigation by Company/Institution · Legal Reasons and/or Threats · Objections by Author(s) · · Correction later updated; P Anversa investigated;
- Commented on by
- Erratum issuedCorrection.2015
- Erratum issuedCorrection.2015
- Expression of concern
- Expression of concern
- Retracted
Authors and funding
11 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundAging negatively impacts on the function of resident human cardiac progenitor cells (hCPCs). Effective regeneration of the injured heart requires mobilization of hCPCs to the sites of damage. In the young heart, signaling by the guidance receptor EphA2 in response to the ephrin A1 ligand promotes hCPC motility and improves cardiac recovery after infarction. METHODS AND
resultsWe report that old hCPCs are characterized by cell-autonomous inhibition of their migratory ability ex vivo and impaired translocation in vivo in the damaged heart. EphA2 expression was not decreased in old hCPCs; however, the elevated level of reactive oxygen species in aged cells induced post-translational modifications of the EphA2 protein. EphA2 oxidation interfered with ephrin A1-stimulated receptor auto-phosphorylation, activation of Src family kinases, and caveolin-1-mediated internalization of the receptor. Cellular aging altered the EphA2 endocytic route, affecting the maturation of EphA2-containing endosomes and causing premature signal termination. Overexpression of functionally intact EphA2 in old hCPCs corrected the defects in endocytosis and downstream signaling, enhancing cell motility. Based on the ability of phenotypically young hCPCs to respond efficiently to ephrin A1, we developed a novel methodology for the prospective isolation of live hCPCs with preserved migratory capacity and growth reserve.
conclusionsOur data demonstrate that the ephrin A1/EphA2 pathway may serve as a target to facilitate trafficking of hCPCs in the senescent myocardium. Importantly, EphA2 receptor function can be implemented for the selection of hCPCs with high therapeutic potential, a clinically relevant strategy that does not require genetic manipulation of stem cells.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.