Evidence map›Paper›PMID 34921407›Full record

ArticleThe Journal of physiology2022

What gets on the nerves of cardiac patients? Pathophysiological changes in cardiac innervation.

Courtney Clyburn, Joseph J Sepe, Beth A Habecker

Open access · hybridAbstract read
In one paragraph

Article in The Journal of physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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  8. Article
  9. Review
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  11. Review
  12. Neurocardiac Axis Physiology and Clinical Applications.International journal of cardiology. Heart & vasculature · 2024
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Stellate Ganglia and Cardiac Sympathetic Overactivation in Heart Failure.International journal of molecular sciences · 2022
    Review
  20. Neurotoxic Effect of Doxorubicin Treatment on Cardiac Sympathetic Neurons.International journal of molecular sciences · 2022
    Article
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

3 authors at 1 institution in 1 country.

Courtney ClyburnDepartment of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, Oregon, USA.ORCID 0000-0003-1300-3705
Joseph J SepeDepartment of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, Oregon, USA.
Beth A HabeckerDepartment of Chemical Physiology and Biochemistry, Oregon Health and Science University, Portland, Oregon, USA.ORCID 0000-0002-4658-8730
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
Peripheral Sympathetic Dysfunction in Cardiac DiseaseR01HL146833 · NHLBI · OREGON HEALTH & SCIENCE UNIVERSITY · PI BETH A HABECKER · 2020 to 2026
$5.1M
NHLBI NIH HHS R01 HL093056NHLBI NIH HHS R01 HL146833
6 · The paper itself

Abstract

The autonomic nervous system regulates cardiac function by balancing the actions of sympathetic and parasympathetic inputs to the heart. Intrinsic cardiac neurocircuits integrate these autonomic signals to fine-tune cardiac control, and sensory feedback loops regulate autonomic transmission in the face of external stimuli. These interconnected neural systems allow the heart to adapt to constantly changing circumstances that range from simple fluctuations in body position to running a marathon. The cardiac reflexes that serve to maintain homeostasis in health are disrupted in many disease states. This is often characterized by increased sympathetic and decreased parasympathetic transmission. Studies of cardiovascular disease reveal remodelling of cardiac neurocircuits at several functional and anatomical levels. Central circuits change so that sympathetic pathways become hyperactive, while parasympathetic circuits exhibit decreased activity. Peripheral sensory nerves also become hyperactive in disease, which increases patients' risk for poor cardiac outcomes. Injury and disease also alter the types of neurotransmitters and neuropeptides released by autonomic nerves in the heart, and can lead to regional hyperinnervation (increased nerve density) or denervation (decreased nerve density) of cardiac tissue. The mechanisms responsible for neural remodelling are not fully understood, but neurotrophins and inflammatory cytokines are likely involved. Areas of active investigation include the role of immune cells and inflammation in neural remodelling, as well as the role of glia in modulating peripheral neuronal activity. Our growing understanding of autonomic dysfunction in disease has facilitated development of new therapeutic strategies to improve health outcomes.

Indexed as

Autonomic Nervous SystemHeartHomeostasisHumansNerve Growth FactorsNeurotransmitter AgentsNerve Growth FactorsNeurotransmitter Agentsautonomic nervous systemcardiacgliainflammationparasympatheticsensory nervessympathetic

Identifiers

PMID34921407
PMCPMC8810748
OpenAlexW4200099915

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.