Evidence map›Paper›PMID 42146601›Full record

ArticlebioRxiv : the preprint server for biology2026

A Perturb-seq screen guided by species divergence uncovers pathways for collateral artery formation.

Xiaochen Fan, Ronghao Zhou, Brian C Raftrey, Pamela E Rios Coronado, Emily Trimm, Erin Clancy, Xinhong Chen, Jamie Bozeman, Maggie S Chen, Shoxruxxon Alimukhamedov and 11 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

21 authors.

Xiaochen FanDepartment of Biology, Stanford University, Stanford, CA, USA.ORCID 0000-0002-4316-0616
Ronghao ZhouDepartment of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
Brian C RaftreyDepartment of Biology, Stanford University, Stanford, CA, USA.
Pamela E Rios CoronadoDepartment of Biology, Stanford University, Stanford, CA, USA.
Emily TrimmBiophysics Program, Stanford University School of Medicine, Stanford, CA, USA.
Erin ClancyInstitute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA, USA.
Xinhong ChenDivision of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA, USA.ORCID 0000-0003-0408-0813
Jamie BozemanDepartment of Biology, Stanford University, Stanford, CA, USA.
Maggie S ChenDepartment of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
Shoxruxxon AlimukhamedovThe Phil and Penny Knight Initiative for Brain Resilience, Stanford University, Stanford, CA, USA.
Juan AlcocerDepartment of Biology, Stanford University, Stanford, CA, USA.
Idalina BonhamCPP Armamentarium Vector Core, California State Polytechnic University, Pomona, CA, USA.
Stuti AgarwalDivision of Pulmonary, Allergy, and Critical Care Medicine, Stanford University School of Medicine, Stanford, CA, USA.
Alina IsakovaThe Phil and Penny Knight Initiative for Brain Resilience, Stanford University, Stanford, CA, USA.ORCID 0000-0003-1113-6889
Vinicio A de Jesus PerezDivision of Pulmonary, Allergy, and Critical Care Medicine, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0001-5532-8247
Chong Y ParkDivision of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, CA, USA.
Timothy F ShayDivision of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA, USA.ORCID 0000-0001-6591-3271
Viviana GradinaruDivision of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA, USA.
Thomas QuertermousDivision of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, CA, USA.ORCID 0000-0002-7645-9067
Jesse M EngreitzStanford Cardiovascular Institute, Stanford University, Stanford, CA, USA.ORCID 0000-0002-5754-1719
Kristy Red-HorseDepartment of Biology, Stanford University, Stanford, CA, USA.

Funding

INSTITUTIONAL TRAINING GRANT IN GENOME SCIENCET32HG000044 · NHGRI · STANFORD UNIVERSITY · PI MICHAEL P. SNYDER · 1995 to 2026
$32.2M
Stanford Center for Connecting DNA Variants to Function and PhenotypeUM1HG011972 · NHGRI · STANFORD UNIVERSITY · PI JESSE M ENGREITZ, THOMAS QUERTERMOUS · 2021 to 2026
$10.5M
Scientific Core: Perturb-seq library generation, sequencing, and data analysisP01HL180323 · NHLBI · STANFORD UNIVERSITY · PI THOMAS QUERTERMOUS · 2025 to 2026
$7.1M
Engineered AAV Identification, Validation, and Dissemination Pipeline for Brain Cell Type-Specific Manipulation Across SpeciesUF1MH128336 · NIMH · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI FOX, ANDREW S, GRADINARU, VIVIANA · 2021 to 2021
$6.1M
Mechanotransduction and transcriptional regulation during artery developmentR01HL128503 · NHLBI · STANFORD UNIVERSITY · PI Mary Red-Horse · 2015 to 2026
$5.8M
Scaled identification of receptor-targeted AAVs for potent and cell type-specific transgene deliveryU01MH139785 · NIMH · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI Andrew S Fox, Viviana Gradinaru · 2025 to 2026
$5.5M
Intersecting clinical, genomic, and experimental investigation to understand the mechanisms and impact of coronary artery patterningR01HL171326 · NHLBI · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI Themistocles L Assimes, Mary Red-Horse · 2024 to 2026
$2.0M
NHGRI NIH HHS T32 HG000044NHGRI NIH HHS UM1 HG011972NHLBI NIH HHS P01 HL180323NHLBI NIH HHS R01 HL128503NHLBI NIH HHS R01 HL171326NIMH NIH HHS U01 MH139785NIMH NIH HHS UF1 MH128336
6 · The paper itself

Abstract

Collateral arteries are natural bypasses that can reroute blood flow around arterial blockages, limiting tissue injury during stroke and coronary artery disease. Despite their clinical effectiveness, therapeutic strategies to stimulate collateral artery growth remain unavailable due to our limited understanding of their developmental mechanisms. Remarkably, guinea pigs display exceptionally dense collateral artery networks across various organs, resulting in complete resistance to ischemic damage in the brain and heart. In this study, we compared single-cell RNA sequencing (scRNA-seq) from guinea pig and mouse tissues to identify endothelial cell (EC) gene expression patterns associated with extensive collateral artery development. We then developed an

Identifiers

PMID42146601
PMCPMC13174509

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.