Evidence map›Paper›PMID 26988631›Full record

ReviewExperimental physiology2016

Glia, sympathetic activity and cardiovascular disease.

Nephtali Marina, Anja G Teschemacher, Sergey Kasparov, Alexander V Gourine

Open access · hybridAbstract readReview
In one paragraph

Review in Experimental physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. The association between enlarged perivascular spaces and muscle sympathetic nerve activity in normotensive and hypertensive humans.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2025
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  18. Unilateral vagotomy alters astrocyte and microglial morphology in the nucleus tractus solitarii of the rat.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
    Article
  19. Article
  20. 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

4 authors at 3 institutions in 1 country.

Nephtali MarinaDepartment of Clinical Pharmacology, University College London, London, WC1E 6JF, UK.
Anja G TeschemacherSchool of Physiology and Pharmacology, Medical Sciences Building, Bristol Heart Institute, University of Bristol, Bristol, BS8 1TD, UK.
Sergey KasparovSchool of Physiology and Pharmacology, Medical Sciences Building, Bristol Heart Institute, University of Bristol, Bristol, BS8 1TD, UK.
Alexander V GourineCentre for Cardiovascular and Metabolic Neuroscience, Neuroscience, Physiology & Pharmacology, University College London, London, WC1E 6BT, UK.
University College London · GBNIHR Bristol Cardiovascular Biomedical Research Unit · GBUniversity of Bristol · GB

Funding

Biotechnology and Biological Sciences Research Council BB/L019396/1British Heart Foundation FS/12/1/29080British Heart Foundation FS/13/5/29927Medical Research Council MR/L020661/1Wellcome Trust
6 · The paper itself

Abstract

NEW

findingsWhat is the topic of this review? In this review, we discuss recent findings that provide a novel insight into the mechanisms that link glial cell function with the pathogenesis of cardiovascular disease, including systemic arterial hypertension and chronic heart failure. What advances does it highlight? We discuss how glial cells may influence central presympathetic circuits, leading to maladaptive and detrimental increases in sympathetic activity and contributing to the development and progression of cardiovascular disease. Increased activity of the sympathetic nervous system is associated with the development of cardiovascular disease and may contribute to its progression. Vasomotor and cardiac sympathetic activities are generated by the neuronal circuits located in the hypothalamus and the brainstem. These neuronal networks receive multiple inputs from the periphery and other parts of the CNS and, at a local level, may be influenced by their non-neuronal neighbours, in particular glial cells. In this review, we discuss recent experimental evidence suggesting that astrocytes and microglial cells are able to modulate the activity of sympathoexcitatory neural networks in disparate physiological and pathophysiological conditions. We focus on the chemosensory properties of astrocytes residing in the rostral ventrolateral medulla oblongata and discuss signalling mechanisms leading to glial activation during brain hypoxia and inflammation. Alterations in these mechanisms may lead to heightened activity of sympathoexcitatory CNS circuits and contribute to maladaptive and detrimental increases in sympathetic tone associated with systemic arterial hypertension and chronic heart failure.

Indexed as

AnimalsCardiovascular DiseasesHumansHypoxiaMedulla OblongataNeurogliaNeuronsSympathetic Nervous System

Identifiers

PMID26988631
PMCPMC5031202
OpenAlexW2297780814

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.