Evidence map›Paper›PMID 26890698›Full record

ReviewThe Journal of physiology2016

Mechanisms of microglial activation in models of inflammation and hypoxia: Implications for chronic intermittent hypoxia.

Elizabeth A Kiernan, Stephanie M C Smith, Gordon S Mitchell, Jyoti J Watters

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

74 citing papers in PubMed, 105 citations in OpenAlex.

  1. Review
  2. Article
  3. Sleep, Neural Circulatory Control, and Cardiovascular Disease: A Mechanistic Review.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  4. Review
  5. Review
  6. Review
  7. Mechanisms underlying end-organ injury in sleep apnoea.The European respiratory journal · 2026
    Review
  8. Article
  9. Article
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  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
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14 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Elizabeth A KiernanDepartment of Comparative Biosciences, University of Wisconsin-Madison, Madison, WI 53706, USA.
Stephanie M C SmithDepartment of Comparative Biosciences, University of Wisconsin-Madison, Madison, WI 53706, USA.
Gordon S MitchellDepartment of Physical Therapy, University of Florida, Gainesville, FL, 32610, USA.
Jyoti J WattersDepartment of Comparative Biosciences, University of Wisconsin-Madison, Madison, WI 53706, USA.
University of Wisconsin–Madison · USUniversity of Florida Health · US

Funding

NEUROSCIENCE TRAINING PROGRAMT32GM007507 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI HALLORAN, MARY C · 1985 to 2017
$9.3M
Intermittent Hypoxia-Induced Inflammation Modulates Respiratory PlasticityR01HL111598 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI MITCHELL, GORDON S., WATTERS, JYOTI J · 2012 to 2016
$2.9M
Oligosaccharides Regulating Cell FunctionR21GM075007 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SASISEKHARAN, RAM · 2005 to 2006
$226k
NHLBI NIH HHS HL07694NHLBI NIH HHS R01 HL111598NIGMS NIH HHS GM0075007NIGMS NIH HHS T32 GM007507
6 · The paper itself

Abstract

Chronic intermittent hypoxia (CIH) is a hallmark of sleep apnoea, a condition associated with diverse clinical disorders. CIH and sleep apnoea are characterized by increased reactive oxygen species formation, peripheral and CNS inflammation, neuronal death and neurocognitive deficits. Few studies have examined the role of microglia, the resident CNS immune cells, in models of CIH. Thus, little is known concerning their direct contributions to neuropathology or the cellular mechanisms regulating their activities during or following pathological CIH. In this review, we identify gaps in knowledge regarding CIH-induced microglial activation, and propose mechanisms based on data from related models of hypoxia and/or hypoxia-reoxygenation. CIH may directly affect microglia, or may have indirect effects via the periphery or other CNS cells. Peripheral inflammation may indirectly activate microglia via entry of pro-inflammatory molecules into the CNS, and/or activation of vagal afferents that trigger CNS inflammation. CIH-induced release of damage-associated molecular patterns from injured CNS cells may also activate microglia via interactions with pattern recognition receptors expressed on microglia. For example, Toll-like receptors activate mitogen-activated protein kinase/transcription factor pathways required for microglial inflammatory gene expression. Although epigenetic effects from CIH have not yet been studied in microglia, potential epigenetic mechanisms in microglial regulation are discussed, including microRNAs, histone modifications and DNA methylation. Epigenetic effects can occur during CIH, or long after it has ended. A better understanding of CIH effects on microglial activities may be important to reverse CIH-induced neuropathology in patients with sleep disordered breathing.

Indexed as

AnimalsHumansHypoxiaInflammationMAP Kinase Signaling SystemMicrogliaSleep Apnea SyndromesToll-Like ReceptorsToll-Like Receptors

Identifiers

PMID26890698
PMCPMC4799985
OpenAlexW2282781293

What OpenQuestion holds

Textmetadata
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.