Evidence map›Paper›PMID 25150828›Full record

ReviewAmerican journal of hypertension2014

The immunological basis of hypertension.

Bernardo Rodríguez-Iturbe, Héctor Pons, Yasmir Quiroz, Richard J Johnson

Abstract readReview
In one paragraph

Review in American journal of hypertension, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

56 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. The Pathophysiological Role of Thymosin β4 in the Kidney Glomerulus.International journal of molecular sciences · 2023
    Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Cytokine Profiles Associated With Acute COVID-19 and Long COVID-19 Syndrome.Frontiers in cellular and infection microbiology · 2022
    Article
  17. Article
  18. 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.

Bernardo Rodríguez-IturbeHospital Universitario y Universidad del Zulia, Maracaibo, Venezuela; Instituto Venezolano de Investigaciones Científicas-Zulia, Maracaibo, Venezuela; brodrigueziturbe@gmail.com.
Héctor PonsHospital Universitario y Universidad del Zulia, Maracaibo, Venezuela;
Yasmir QuirozInstituto Venezolano de Investigaciones Científicas-Zulia, Maracaibo, Venezuela;
Richard J JohnsonDivision of Renal Diseases and Hypertension, University of Colorado, Denver, Colorado.

Funding

Role of Uric Acid in Hypertension and Renal DiseaseR01HL068607 · NHLBI · UNIVERSITY OF FLORIDA · PI JOHNSON, RICHARD JOSEPH · 2002 to 2011
$3.5M
NHLBI NIH HHS HL-68607NHLBI NIH HHS R01 HL068607
6 · The paper itself

Abstract

A large number of investigations have demonstrated the participation of the immune system in the pathogenesis of hypertension. Studies focusing on macrophages and Toll-like receptors have documented involvement of the innate immunity. The requirements of antigen presentation and co-stimulation, the critical importance of T cell-driven inflammation, and the demonstration, in specific conditions, of agonistic antibodies directed to angiotensin II type 1 receptors and adrenergic receptors support the role of acquired immunity. Experimental findings support the concept that the balance between T cell-induced inflammation and T cell suppressor responses is critical for the regulation of blood pressure levels. Expression of neoantigens in response to inflammation, as well as surfacing of intracellular immunogenic proteins, such as heat shock proteins, could be responsible for autoimmune reactivity in the kidney, arteries, and central nervous system. Persisting, low-grade inflammation in these target organs may lead to impaired pressure natriuresis, an increase in sympathetic activity, and vascular endothelial dysfunction that may be the cause of chronic elevation of blood pressure in essential hypertension.

Indexed as

Adaptive ImmunityBlood PressureImmunity, InnateAnimalsAutoantibodiesAutoantigensHumansHypertensionInflammationInflammation MediatorsSignal TransductionAutoantibodiesAutoantigensInflammation Mediatorsautoimmunityblood pressurehypertensionimmunitylymphocytesmacrophages.

Identifiers

PMID25150828
PMCPMC4263946

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.