Evidence map›Paper›PMID 27504807›Full record

ArticleeLife2016

Suppression of ischemia in arterial occlusive disease by JNK-promoted native collateral artery development.

Kasmir Ramo, Koichi Sugamura, Siobhan Craige, John F Keaney, Roger J Davis

Open access · goldAbstract read
In one paragraph

Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Genetic determinants of insufficiency of the collateral circulation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. JNK and cardiometabolic dysfunction.Bioscience reports · 2019
    Review
  11. Article
  12. Mixed lineage kinase-3 prevents cardiac dysfunction and structural remodeling with pressure overload.American journal of physiology. Heart and circulatory physiology · 2019
    Article
  13. Review
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

5 authors at 2 institutions in 1 country.

Kasmir RamoProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, United States.
Koichi SugamuraCardiovascular Medicine Division, University of Massachusetts Medical School, Worcester, United States.
Siobhan CraigeCardiovascular Medicine Division, University of Massachusetts Medical School, Worcester, United States.
John F KeaneyCardiovascular Medicine Division, University of Massachusetts Medical School, Worcester, United States.
Roger J DavisProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, United States.ORCID 0000-0002-0130-1652
University of Massachusetts Chan Medical School · USHoward Hughes Medical Institute · US

Funding

Nox4 and Vascular HomeostasisR01HL098407 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KEANEY, JOHN FRANCIS · 2010 to 2017
$3.8M
Metabolic Stress SignalingR01DK107220 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI DAVIS, ROGER J. · 2016 to 2023
$3.6M
Request for SCANCO micro-CT 40 Multi-User Bone StudiesS10RR023540 · NCRR · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI LIAN, JANE B. · 2008 to 2008
$277k
Howard Hughes Medical InstituteNCRR NIH HHS S10 RR023540NHLBI NIH HHS R01 HL098407NIDDK NIH HHS R01 DK107220
6 · The paper itself

Abstract

Arterial occlusive diseases are major causes of morbidity and mortality. Blood flow to the affected tissue must be restored quickly if viability and function are to be preserved. We report that disruption of the mixed-lineage protein kinase (MLK) - cJun NH2-terminal kinase (JNK) signaling pathway in endothelial cells causes severe blockade of blood flow and failure to recover in the murine femoral artery ligation model of hindlimb ischemia. We show that the MLK-JNK pathway is required for the formation of native collateral arteries that can restore circulation following arterial occlusion. Disruption of the MLK-JNK pathway causes decreased Dll4/Notch signaling, excessive sprouting angiogenesis, and defects in developmental vascular morphogenesis. Our analysis demonstrates that the MLK-JNK signaling pathway is a key regulatory mechanism that protects against ischemia in arterial occlusive disease.

Indexed as

MAP Kinase Signaling SystemNeovascularization, PhysiologicAnimalsArterial Occlusive DiseasesDisease Models, AnimalFemoral ArteryIschemiaMAP Kinase Kinase KinasesMiceMorphogenesisMAP Kinase Kinase Kinasesangiogenesiscell biologycollateral arteriescollaterogenesisdevelopmental biologyJNKMLKmousestem cells

Identifiers

PMID27504807
PMCPMC4999312
OpenAlexW2517304751

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.