Evidence map›Paper›PMID 30686582›Full record

ArticleCell2019

A Unique Collateral Artery Development Program Promotes Neonatal Heart Regeneration.

Soumyashree Das, Andrew B Goldstone, Hanjay Wang, Justin Farry, Gaetano D'Amato, Michael J Paulsen, Anahita Eskandari, Camille E Hironaka, Ragini Phansalkar, Bikram Sharma and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed
11.1field-weighted citation impact, top 1% 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

145 citing papers in PubMed, 224 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Mechanisms and Therapeutic Potential of Human Cardiomyocyte Proliferation.Journal of cardiovascular development and disease · 2026
    Review
  11. Article
  12. Partial Deletion ofeNeuro · 2026
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Sirt4 Deficiency Promotes Cardiomyocyte Proliferation and Cardiac Repair.Journal of cellular and molecular medicine · 2025
    Article
  19. Article
  20. Feto-placental blood vessel development.Development (Cambridge, England) · 2025
    Review

85 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 3 institutions in 1 country.

Soumyashree DasDepartment of Biology, Stanford University, Stanford, CA 94305, USA.
Andrew B GoldstoneDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Hanjay WangDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Justin FarryDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Gaetano D'AmatoDepartment of Biology, Stanford University, Stanford, CA 94305, USA.
Michael J PaulsenDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Anahita EskandariDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Camille E HironakaDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA.
Ragini PhansalkarDepartment of Biology, Stanford University, Stanford, CA 94305, USA; Department of Genetics, Stanford University, Stanford, CA 94305, USA.
Bikram SharmaDepartment of Biology, Ball State University, Muncie, IN 47306, USA.
Siyeon RheeDepartment of Biology, Stanford University, Stanford, CA 94305, USA.
Elya Ali ShamskhouDepartment of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.
Dritan AgalliuDepartments of Neurology, Pathology and Cell Biology, and Pharmacology, Columbia University Irving Medical Center, New York, NY 10032, USA.
Vinicio de Jesus PerezDepartment of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.
Y Joseph WooDepartment of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: joswoo@stanford.edu.
Kristy Red-HorseDepartment of Biology, Stanford University, Stanford, CA 94305, USA; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: kredhors@stanford.edu.
Stanford University · USBall State University · USColumbia University Irving Medical Center · US

Funding

ANGIOGENIC TISSUE ENGINEERING TO LIMIT POST-INFARCTION VENTRICULAR REMODELINGR01HL089315 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI WOO, Y JOSEPH · 2008 to 2023
$6.4M
Mechanotransduction and transcriptional regulation during artery developmentR01HL128503 · NHLBI · STANFORD UNIVERSITY · PI Mary Red-Horse · 2015 to 2026
$5.8M
The Wnt7a/ROR2 axis in the pathogenesis of pulmonary arterial hypertensionR01HL134776 · NHLBI · STANFORD UNIVERSITY · PI DE JESUS PEREZ, VINICIO A · 2017 to 2025
$5.0M
Endothelial-pericyte interactions in the pathogenesis of pulmonary arterial hypertensionR01HL139664 · NHLBI · STANFORD UNIVERSITY · PI DE JESUS PEREZ, VINICIO A · 2018 to 2025
$4.7M
Cellular and humoral immune mechanisms underlying neurovascular dysfunction in autoimmune encephalitisR01MH112849 · NIMH · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI AGALLIU, DRITAN, CUTFORTH, TYLER · 2017 to 2020
$2.1M
miR regulation of the neurovasculature function in health and diseaseR01NS107344 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI PEDERSEN, IRENE MUNK · 2018 to 2021
$1.7M
Developing a microfluidic human neurovascular unit system to investigate genetic and age-related risk factors in Alzheimer's diseaseR01AG078352 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Dritan Agalliu, Andrew Alexander Sproul · 2025 to 2026
$837k
NHLBI NIH HHS R01 HL089315NHLBI NIH HHS R01 HL128503NHLBI NIH HHS R01 HL134776NHLBI NIH HHS R01 HL139664NIA NIH HHS R01 AG078352NIMH NIH HHS R01 MH112849NINDS NIH HHS R01 NS107344
6 · The paper itself

Abstract

Collateral arteries are an uncommon vessel subtype that can provide alternate blood flow to preserve tissue following vascular occlusion. Some patients with heart disease develop collateral coronary arteries, and this correlates with increased survival. However, it is not known how these collaterals develop or how to stimulate them. We demonstrate that neonatal mouse hearts use a novel mechanism to build collateral arteries in response to injury. Arterial endothelial cells (ECs) migrated away from arteries along existing capillaries and reassembled into collateral arteries, which we termed "artery reassembly". Artery ECs expressed CXCR4, and following injury, capillary ECs induced its ligand, CXCL12. CXCL12 or CXCR4 deletion impaired collateral artery formation and neonatal heart regeneration. Artery reassembly was nearly absent in adults but was induced by exogenous CXCL12. Thus, understanding neonatal regenerative mechanisms can identify pathways that restore these processes in adults and identify potentially translatable therapeutic strategies for ischemic heart disease.

Indexed as

AnimalsAnimals, NewbornChemokine CXCL12Collateral CirculationCoronary VesselsEndothelial CellsFemaleHeartHumansMaleMiceMice, Inbred C57BLNeovascularization, PhysiologicReceptors, CXCR4RegenerationSignal TransductionChemokine CXCL12CXCL12 protein, humanCxcl12 protein, mouseCXCR4 protein, humanCXCR4 protein, mouseReceptors, CXCR4arterializationarteriogenesiscollateral arteriesCXCL12endothelial cellsheart regenerationmyocardial infarction

Identifiers

PMID30686582
PMCPMC6435282
OpenAlexW2912575300

What OpenQuestion holds

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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.