Evidence map›Paper›PMID 36362099›Full record

ReviewInternational journal of molecular sciences2022

Stellate Ganglia and Cardiac Sympathetic Overactivation in Heart Failure.

Yu-Long Li

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 2% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Channels (Austin, Tex.) · 2026
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  12. Electrophysiological comparison of left versus right stellate ganglia neurons.Journal of molecular and cellular cardiology plus · 2025
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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

1 author at 1 institution in 1 country.

Yu-Long LiDepartment of Emergency Medicine, University of Nebraska Medical Center, Omaha, NE 68198, USA.
University of Nebraska Medical Center · US

Funding

Mechanisms of cardiac sympathetic hyperactivity in chronic heart failureR01HL137832 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Yu-Long Li · 2017 to 2026
$4.1M
Potential therapies to improve ventricular vagal function in type 2 diabetesR01HL144146 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI LI, YU-LONG · 2018 to 2021
$1.5M
NHLBI NIH HHS R01 HL137832NHLBI NIH HHS R01 HL144146NIH HHS R01HL-137832NIH HHS R01HL-144146
6 · The paper itself

Abstract

Heart failure (HF) is a major public health problem worldwide, especially coronary heart disease (myocardial infarction)-induced HF with reduced ejection fraction (HFrEF), which accounts for over 50% of all HF cases. An estimated 6 million American adults have HF. As a major feature of HF, cardiac sympathetic overactivation triggers arrhythmias and sudden cardiac death, which accounts for nearly 50-60% of mortality in HF patients. Regulation of cardiac sympathetic activation is highly integrated by the regulatory circuitry at multiple levels, including afferent, central, and efferent components of the sympathetic nervous system. Much evidence, from other investigators and us, has confirmed the afferent and central neural mechanisms causing sympathoexcitation in HF. The stellate ganglion is a peripheral sympathetic ganglion formed by the fusion of the 7th cervical and 1st thoracic sympathetic ganglion. As the efferent component of the sympathetic nervous system, cardiac postganglionic sympathetic neurons located in stellate ganglia provide local neural coordination independent of higher brain centers. Structural and functional impairments of cardiac postganglionic sympathetic neurons can be involved in cardiac sympathetic overactivation in HF because normally, many effects of the cardiac sympathetic nervous system on cardiac function are mediated via neurotransmitters (e.g., norepinephrine) released from cardiac postganglionic sympathetic neurons innervating the heart. This review provides an overview of cardiac sympathetic remodeling in stellate ganglia and potential mechanisms and the role of cardiac sympathetic remodeling in cardiac sympathetic overactivation and arrhythmias in HF. Targeting cardiac sympathetic remodeling in stellate ganglia could be a therapeutic strategy against malignant cardiac arrhythmias in HF.

Indexed as

Heart FailureStellate GanglionArrhythmias, CardiacHeartHumansStroke VolumeSympathetic Nervous Systemarrhythmiaautonomic nervous systemcardiac sympathetic activationheart failureinflammationstellate ganglion

Identifiers

PMID36362099
PMCPMC9653702
OpenAlexW4308122984

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.