Evidence map›Paper›PMID 34689174›Full record

ReviewJournal of human hypertension2022

Innate immunity and clinical hypertension.

Justin P Van Beusecum, Hietor Moreno, David G Harrison

Open access · greenAbstract readReview
In one paragraph

Review in Journal of human hypertension, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Gut bacteria-derived extracellular vesicles and hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Male kidney-specific BMAL1 knockout mice are protected from KAmerican journal of physiology. Renal physiology · 2023
    Article
  17. Review
  18. Review
  19. Sodium Homeostasis and Hypertension.Current cardiology reports · 2023
    Review
  20. Life is really simple, but we insist on making it complicated. (Confucius).Hypertension research : official journal of the Japanese Society of Hypertension · 2023
    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

3 authors at 3 institutions in 2 countries.

Justin P Van BeusecumDivision of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.ORCID 0000-0002-9265-9915
Hietor MorenoDepartment of Internal Medicine, Faculty of Medical Sciences, Cardiovascular Pharmacology Laboratory, University of Campinas, Campinas, Brazil.ORCID 0000-0001-6330-697X
David G HarrisonDivision of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA. David.g.harrison@vumc.org.ORCID 0000-0001-9363-6451
Medical University of South Carolina · USUniversidade Estadual de Campinas (UNICAMP) · BRVanderbilt University · US

Funding

The Role of Inflammation in Cardiovascular DiseaseP01HL129941 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HARRISON, DAVID G · 2016 to 2020
$12.4M
Mechanisms of Immune Activation in HypertensionR35HL140016 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HARRISON, DAVID G · 2018 to 2024
$5.3M
A Role of GAS6/Axl Signaling in the Development of Essential HypertensionIK2BX005605 · VA · VETERANS HEALTH ADMINISTRATION · PI VAN BEUSECUM, JUSTIN PIETER · 2021 to 2025
–
BLRD VA IK2 BX005605NHLBI NIH HHS P01 HL129941NHLBI NIH HHS R35 HL140016U.S. Department of Health & Human Services | National Institutes of Health (NIH) R35HL140016U.S. Department of Health and Human Services (U.S. Department of Health & Human Services) P01HL12994U.S. Department of Veterans Affairs (Department of Veterans Affairs) CDA IK2 BX005605
6 · The paper itself

Abstract

Emerging evidence has supported a role of inflammation and immunity in the genesis of hypertension. In humans and experimental models of hypertension, cells of the innate and adaptive immune system enter target tissues, including vessels and the kidney, and release powerful mediators including cytokines, matrix metalloproteinases and reactive oxygen species that cause tissue damage, fibrosis and dysfunction. These events augment the blood pressure elevations in hypertension and promote end-organ damage. Factors that activate immune cells include sympathetic outflow, increased sodium within microenvironments where these cells reside, and signals received from the vasculature. In particular, the activated endothelium releases reactive oxygen species and interleukin (IL)-6 which in turn stimulate transformation of monocytes to become antigen presenting cells and produce cytokines like IL-1β and IL-23, which further affect T cell function to produce IL-17A. Genetic deletion or neutralization of these cytokines ameliorates hypertension and end-organ damage. In this review, we will consider in depth features of the hypertensive milieu that lead to these events and consider new treatment approaches to limit the untoward effects of inflammation in hypertension.

Indexed as

HypertensionCytokinesHumansImmunity, InnateInflammationReactive Oxygen SpeciesT-LymphocytesCytokinesReactive Oxygen Species

Identifiers

PMID34689174
PMCPMC9125746
OpenAlexW3211021611

What OpenQuestion holds

Textmetadata
LicenceTDM
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.