Evidence map›Paper›PMID 30117098›Full record

ReviewCellular and molecular neurobiology2019

Mineralocorticoid Receptors, Neuroinflammation and Hypertensive Encephalopathy.

Maria Elvira Brocca, Luciana Pietranera, Edo Ronald de Kloet, Alejandro Federico De Nicola

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

13 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Treatment withNutrients · 2024
    Article
  4. Review
  5. Review
  6. Article
  7. Article
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  9. Review
  10. Review
  11. Article
  12. Article
  13. Introduction to the Special Issue "Neuroactive Steroids".Cellular and molecular neurobiology · 2019
    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 3 countries.

Maria Elvira BroccaLaboratory of Neuroendocrine Biochemistry, Instituto de Biologia y Medicina Experimental-CONICET, Buenos Aires, Argentina.
Luciana PietraneraLaboratory of Neuroendocrine Biochemistry, Instituto de Biologia y Medicina Experimental-CONICET, Buenos Aires, Argentina.
Edo Ronald de KloetDivision of Endocrinology, Department of Internal Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Alejandro Federico De NicolaLaboratory of Neuroendocrine Biochemistry, Instituto de Biologia y Medicina Experimental-CONICET, Buenos Aires, Argentina. alejandrodenicola@gmail.com.ORCID http://orcid.org/0000-0002-3523-9148
Consejo Nacional de Investigaciones Científicas y Técnicas · ARLeiden University Medical Center · NLUniversidad de Buenos Aires · AR

Funding

Consejo Nacional de Investigaciones Científicas y Técnicas PIP 11220170100002COMinisterio de Ciencia, Tecnología e Innovación Productiva PICT 0009Ministerio de Ciencia, Tecnología e Innovación Productiva PICT 0820Secretaria de Ciencia y Tecnica, Universidad de Buenos Aires Ubacyt 418BA
6 · The paper itself

Abstract

Worldwide, raised blood pressure is estimated to affect 35-40% of the adult population and is a main conditioning factor for cardiovascular diseases and stroke. Animal models of hypertension have provided great advances concerning the pathophysiology of human hypertension, as already shown for the deoxycorticosterone-salt treated rat, the Dahl-salt sensitive rat, the Zucker obese rat and the spontaneously hypertensive rat (SHR). SHR has been widely used to study abnormalities of the brain in chronic hypertension. This review summarises present and past evidence that in the SHR, hypertension causes hippocampal tissue damage which triggers a pro-inflammatory feedforward cascade affecting this vulnerable brain region. The cascade is driven by mineralocorticoid receptor (MR) activation responding to endogenous corticosterone rather than aldosterone. Increased MR expression is a generalised feature of the SHR which seems to support first the rise in blood pressure. Then oxidative stress caused by vasculopathy and hypoxia further increases MR activation in hippocampal neurons and glia cells, activates microglia activation and pro-inflammatory mediators, and down-regulates anti-inflammatory factors. In contrast to MR, involvement of the glucocorticoid receptor (GR) in SHR is less certain. GR showed normal expression levels and blockage with an antagonist failed to reduce blood pressure of SHR. The findings support the concept that MR:GR imbalance caused by vasculopathy causes a switch in MR function towards a proverbial "death" receptor.

Indexed as

AnimalsDisease Models, AnimalHumansHypertensive EncephalopathyInflammationNervous SystemReceptors, GlucocorticoidReceptors, MineralocorticoidReceptors, GlucocorticoidReceptors, MineralocorticoidHypertensionMicrogliaMineralocorticoid receptorNeuroinflammation

Identifiers

PMID30117098
PMCPMC11469880
OpenAlexW2887625728

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.