Evidence map›Paper›PMID 25015967›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2014

Tumor necrosis factor-α inhibition attenuates middle cerebral artery remodeling but increases cerebral ischemic damage in hypertensive rats.

Paulo W Pires, Saavia S Girgla, Guillermo Moreno, Jonathon L McClain, Anne M Dorrance

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.6field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Tumor Necrosis Factor-Disease markers · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Correlations of C-Reactive Protein (CRP), Interleukin-6 (IL-6), and Insulin Resistance with Cerebral Infarction in Hypertensive Patients.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Cerebral microhemorrhages: mechanisms, consequences, and prevention.American journal of physiology. Heart and circulatory physiology · 2017
    Review
  17. Article
  18. Review
  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

5 authors at 1 institution in 1 country.

Paulo W PiresDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan pwpires@gmail.com.
Saavia S GirglaDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan.
Guillermo MorenoDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan.
Jonathon L McClainDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan.
Anne M DorranceDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan.
Michigan State University · US

Funding

Spartan MARC U-START34GM100872 · NIGMS · MICHIGAN STATE UNIVERSITY · PI SISK, CHERYL L. · 2013 to 2016
$568k
NIGMS NIH HHS T34 GM100872
6 · The paper itself

Abstract

Hypertension causes vascular inflammation evidenced by an increase in perivascular macrophages and proinflammatory cytokines in the arterial wall. Perivascular macrophage depletion reduced tumor necrosis factor (TNF)-α expression in cerebral arteries of hypertensive rats and attenuated inward remodeling, suggesting that TNF-α might play a role in the remodeling process. We hypothesized that TNF-α inhibition would improve middle cerebral artery (MCA) structure and reduce damage after cerebral ischemia in hypertensive rats. Six-week-old male stroke-prone spontaneously hypertensive rats (SHRSP) were treated with the TNF-α inhibitor etanercept (ETN; 1.25 mg·kg(-1)·day(-1) ip daily) or PBS (equivolume) for 6 wk. The myogenic tone generation, postischemic dilation, and passive structure of MCAs were assessed by pressure myography. Cerebral ischemia was induced by MCA occlusion (MCAO). Myogenic tone was unchanged, but MCAs from SHRSP + ETN had larger passive lumen diameter and reduced wall thickness and wall-to-lumen ratio. Cerebral infarct size was increased in SHRSP + ETN after transient MCAO, despite an improvement in dilation of nonischemic MCA. The increase in infarct size was linked to a reduction in the number of microglia in the infarct core and upregulation of markers of classical macrophage/microglia polarization. There was no difference in infarct size after permanent MCAO or when untreated SHRSP subjected to transient MCAO were given ETN at reperfusion. Our data suggests that TNF-α inhibition attenuates hypertensive MCA remodeling but exacerbates cerebral damage following ischemia/reperfusion injury likely due to inhibition of the innate immune response of the brain.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalBlood PressureEtanerceptHypertensionImmunoglobulin GInfarction, Middle Cerebral ArteryMacrophagesMaleMicrogliaMiddle Cerebral ArteryRatsRats, Inbred SHRReceptors, Tumor Necrosis FactorTumor Necrosis Factor-alphaVasodilationAnti-Inflammatory Agents, Non-SteroidalEtanerceptImmunoglobulin GReceptors, Tumor Necrosis FactorTumor Necrosis Factor-alphacerebral vascular remodelinghypertensionischemic strokemacrophages/microgliatumor necrosis factor-α

Identifiers

PMID25015967
PMCPMC4280151
OpenAlexW2005332632

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.