Evidence map›Paper›PMID 23097471›Full record

ArticleAmerican journal of physiology. Renal physiology2013

Immune reactivity to heat shock protein 70 expressed in the kidney is cause of salt-sensitive hypertension.

Héctor Pons, Atilio Ferrebuz, Yasmir Quiroz, Freddy Romero-Vasquez, Gustavo Parra, Richard J Johnson, Bernardo Rodriguez-Iturbe

Abstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

64 citing papers in PubMed, 102 citations in OpenAlex.

  1. Review
  2. Review
  3. Oxidative Stress in Heat Stress Nephropathy: Crosstalk.Oxidative medicine and cellular longevity · 2026
    Review
  4. Immunology of Hypertension: Pathophysiological and Therapeutic Aspects.International journal of molecular sciences · 2025
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Pathophysiology of primary hypertension in children and adolescents.Pediatric nephrology (Berlin, Germany) · 2024
    Review
  10. Review
  11. Long Noncoding RNA MALAT1: Salt-Sensitive Hypertension.International journal of molecular sciences · 2024
    Review
  12. The damaging duo: Obesity and excess dietary salt contribute to hypertension and cardiovascular disease.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2023
    Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Current Understanding of Pressure Natriuresis.Electrolyte & blood pressure : E & BP · 2021
    Review

4 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

7 authors at 3 institutions in 2 countries.

Héctor PonsHospital Universitario y Universidad del Zulia, Maracaibo, Venezuela.
Atilio Ferrebuz
Yasmir Quiroz
Freddy Romero-Vasquez
Gustavo Parra
Richard J Johnson
Bernardo Rodriguez-Iturbe
Instituto Venezolano de Investigaciones Científicas · VEUniversity of Zulia · VEUniversity of Colorado Denver · US

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-68607
6 · The paper itself

Abstract

Hypertension affects one-third of the adult population of the world. The causes of hypertension are incompletely understood, but relative impairment of sodium excretion is central to its pathogenesis. Immune cell infiltration in the kidney is a constant finding in hypertension that in association with local angiotensin and oxidants causes a defect in sodium excretion. However, it is unclear if the T cell influx into the kidney responds to nonspecific chemokine cues or is due to antigen-driven immune attraction. We found that T cells in experimentally induced salt-driven hypertension present a CD4 clonal response to heat shock protein 70 (HSP70) that is overexpressed in the kidney. We used a highly preserved amino acid sequence within the HSP molecule to induce immune tolerance associated with the generation of IL-10 producing regulatory T cells. Immune tolerant rats to HSP70 developed minimal renal inflammation and were protected from the development of salt-sensitive hypertension. Adoptive transfer of T lymphocytes isolated from spleen of tolerized rats also reversed hypertension. HSP70 gene delivery to the renal vein of the kidneys of rats sensitized to HSP70 caused an increment in blood pressure in response to a high-salt diet. The HSP70 peptide used in this work induces a strong proliferative response in peripheral blood lymphocytes of patients with essential hypertension. These studies provide evidence that autoimmunity plays a role in salt-sensitive hypertension and identifies HSP70 expressed in the kidney as one key antigen. These findings raise the possibility of novel approaches to the treatment of this condition.

Indexed as

AdultAnimalsAutoimmunityBlood PressureCD4-Positive T-LymphocytesCell MovementCell ProliferationCells, CulturedDisease Models, AnimalFemaleHSP70 Heat-Shock ProteinsHumansHypertensionInterleukin-10KidneyMaleHSP70 Heat-Shock ProteinsInterleukin-10Sodium Chloride, Dietary

Identifiers

PMID23097471
PMCPMC3566521
OpenAlexW1969434818

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.