Evidence map›Paper›PMID 25377552›Full record

ArticleDevelopment (Cambridge, England)2014

The sinus venosus contributes to coronary vasculature through VEGFC-stimulated angiogenesis.

Heidi I Chen, Bikram Sharma, Brynn N Akerberg, Harri J Numi, Riikka Kivelä, Pipsa Saharinen, Haig Aghajanian, Andrew S McKay, Patrick E Bogard, Andrew H Chang and 5 more

Open access · greenAbstract read
In one paragraph

Article in Development (Cambridge, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

141 citing papers in PubMed, 1 synthesis or guideline pooled it, 231 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Angiogenic Doping: Plausible Yet Difficult to Detect.Sports medicine (Auckland, N.Z.) · 2026
    Review
  4. Article
  5. Journal of cardiovascular development and disease · 2026
    Article
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81 more citing papers are in PubMed but not listed here.

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

15 authors at 5 institutions in 2 countries.

Heidi I ChenDepartment of Biological Sciences, Stanford University, Stanford, CA 94305, USA.
Bikram SharmaDepartment of Biological Sciences, Stanford University, Stanford, CA 94305, USA.
Brynn N AkerbergInstitute of Molecular Biology, University of Oregon, Eugene, OR 97403, USA.
Harri J NumiWihuri Research Institute and Translational Cancer Biology Program, University of Helsinki, Biomedicum Helsinki, 00290 Helsinki, Finland.
Riikka KiveläWihuri Research Institute and Translational Cancer Biology Program, University of Helsinki, Biomedicum Helsinki, 00290 Helsinki, Finland.
Pipsa SaharinenWihuri Research Institute and Translational Cancer Biology Program, University of Helsinki, Biomedicum Helsinki, 00290 Helsinki, Finland.
Haig AghajanianDepartment of Cell and Developmental Biology, The Cardiovascular Institute and Institute for Regenerative Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Andrew S McKayDepartment of Biological Sciences, Stanford University, Stanford, CA 94305, USA.
Patrick E BogardAriosa Diagnostics, Inc., San Jose, CA 95138, USA.
Andrew H ChangDepartment of Biological Sciences, Stanford University, Stanford, CA 94305, USA Department of Developmental Biology, School of Medicine, Stanford University, Stanford, CA 94305, USA.
Andrew H JacobsDepartment of Biological Sciences, Stanford University, Stanford, CA 94305, USA.
Jonathan A EpsteinDepartment of Cell and Developmental Biology, The Cardiovascular Institute and Institute for Regenerative Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Kryn StankunasInstitute of Molecular Biology, University of Oregon, Eugene, OR 97403, USA.
Kari AlitaloWihuri Research Institute and Translational Cancer Biology Program, University of Helsinki, Biomedicum Helsinki, 00290 Helsinki, Finland.
Kristy Red-HorseDepartment of Biological Sciences, Stanford University, Stanford, CA 94305, USA kredhors@stanford.edu.
Stanford University · USUniversity of Helsinki · FIUniversity of Oregon · USUniversity of Pennsylvania · USWihuri Research Institute · FI

Funding

GENETICS TRAINING PROGRAM FOR PHD CANDIDATEST32GM007790 · NIGMS · STANFORD UNIVERSITY · PI BRUNET, ANNE, KINGSLEY, DAVID M · 1985 to 2020
$12.8M
Chromatin Regulation of Heart Valve DevelopmentR01HL115294 · NHLBI · UNIVERSITY OF OREGON · PI STANKUNAS, KRYN · 2014 to 2018
$1.8M
Semaphorin3d and anomalous pulmonary venous returnR01HL118768 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI EPSTEIN, JONATHAN A. · 2013 to 2016
$1.6M
NICHD R25 Summer Research Program at the University of OregonR25HD070817 · NICHD · UNIVERSITY OF OREGON · PI EISEN, JUDITH S · 2011 to 2021
$1.1M
European Research Council 268804NHLBI NIH HHS R01 HL115294NHLBI NIH HHS R01 HL118768NICHD NIH HHS R25 HD070817
6 · The paper itself

Abstract

Identifying coronary artery progenitors and their developmental pathways could inspire novel regenerative treatments for heart disease. Multiple sources of coronary vessels have been proposed, including the sinus venosus (SV), endocardium and proepicardium, but their relative contributions to the coronary circulation and the molecular mechanisms regulating their development are poorly understood. We created an ApjCreER mouse line as a lineage-tracing tool to map SV-derived vessels onto the heart and compared the resulting lineage pattern with endocardial and proepicardial contributions to the coronary circulation. The data showed a striking compartmentalization to coronary development. ApjCreER-traced vessels contributed to a large number of arteries, capillaries and veins on the dorsal and lateral sides of the heart. By contrast, untraced vessels predominated in the midline of the ventral aspect and ventricular septum, which are vessel populations primarily derived from the endocardium. The proepicardium gave rise to a smaller fraction of vessels spaced relatively uniformly throughout the ventricular walls. Dorsal (SV-derived) and ventral (endocardial-derived) coronary vessels developed in response to different growth signals. The absence of VEGFC, which is expressed in the epicardium, dramatically inhibited dorsal and lateral coronary growth but left vessels on the ventral side unaffected. We propose that complementary SV-derived and endocardial-derived migratory routes unite to form the coronary vasculature and that the former requires VEGFC, revealing its role as a tissue-specific mediator of blood endothelial development.

Indexed as

AnimalsCell LineageCell MovementCoronary VesselsHeart AtriaImmunohistochemistryIn Situ HybridizationMiceMice, Mutant StrainsMicroscopy, FluorescenceNeovascularization, PhysiologicVascular Endothelial Growth Factor CVascular Endothelial Growth Factor Cvascular endothelial growth factor C, mouseAngiogenesisApelin receptor (APJAPLNR)Coronary vessel developmentEndotheliumSinus venosusVEGF-C

Identifiers

PMID25377552
PMCPMC4302936
OpenAlexW2093842837

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.