Evidence map›Paper›PMID 23616527›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Infarct-derived chondroitin sulfate proteoglycans prevent sympathetic reinnervation after cardiac ischemia-reperfusion injury.

Ryan T Gardner, Beth A Habecker

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 2 pooled it
2.7field-weighted citation impact, top 10% 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

48 citing papers in PubMed, 2 syntheses or guidelines pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Guidelines for experimental models of myocardial ischemia and infarction.American journal of physiology. Heart and circulatory physiology · 2018
    Guideline
  3. Review
  4. Review
  5. Article
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  8. Review
  9. Hypertension-induced heart failure disrupts cardiac sympathetic innervation.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Autonomic control of ventricular function in health and disease: current state of the art.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2023
    Review
  15. Article
  16. Article
  17. Article
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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

2 authors at 1 institution in 1 country.

Ryan T GardnerDepartment of Physiology and Pharmacology, Neuroscience Graduate Program, Oregon Health and Science University, Portland, Oregon 97239, USA.
Beth A Habecker
Oregon Health & Science University · US

Funding

Neurotrophins and post-infarct plasticity in cardiac sympathetic neuronsR01HL093056 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI BETH A HABECKER · 2009 to 2026
$7.9M
NHLBI NIH HHS HL093056NHLBI NIH HHS R01 HL093056
6 · The paper itself

Abstract

Sympathetic nerves can regenerate after injury to reinnervate target tissues. Sympathetic regeneration is well documented after chronic cardiac ischemia, so we were surprised that the cardiac infarct remained denervated following ischemia-reperfusion (I-R). We used mice to ask if the lack of sympathetic regeneration into the scar was due to blockade by inhibitory extracellular matrix within the infarct. We found that chondroitin sulfate proteoglycans (CSPGs) were present in the infarct after I-R, but not after chronic ischemia, and that CSPGs caused inhibition of sympathetic axon outgrowth in vitro. Ventricle explants after I-R and chronic ischemia stimulated sympathetic axon outgrowth that was blocked by nerve growth factor antibodies. However, growth in I-R cocultures was asymmetrical, with axons growing toward the heart tissue consistently shorter than axons growing in other directions. Growth toward I-R explants was rescued by adding chondroitinase ABC to the cocultures, suggesting that I-R infarct-derived CSPGs prevented axon extension. Sympathetic ganglia lacking protein tyrosine phosphatase sigma (PTPRS) were not inhibited by CSPGs or I-R explants in vitro, suggesting PTPRS is the major CSPG receptor in sympathetic neurons. To test directly if infarct-derived CSPGs prevented cardiac reinnervation, we performed I-R in ptprs-/- and ptprs+/- mice. Cardiac infarcts in ptprs-/- mice were hyperinnervated, while infarcts in ptprs+/- littermates were denervated, confirming that CSPGs prevent sympathetic reinnervation of the cardiac scar after I-R. This is the first example of CSPGs preventing sympathetic reinnervation of an autonomic target following injury, and may have important consequences for cardiac function and arrhythmia susceptibility after myocardial infarction.

Indexed as

AnimalsChondroitin Sulfate ProteoglycansCoculture TechniquesFemaleHeartMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, TransgenicMyocardial InfarctionMyocardial Reperfusion InjuryOrgan Culture TechniquesSympathetic Fibers, PostganglionicChondroitin Sulfate Proteoglycans

Identifiers

PMID23616527
PMCPMC3671889
OpenAlexW1982439010

What OpenQuestion holds

Textmetadata
LicenceTDM
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.