Evidence map›Paper›PMID 26830047›Full record

ReviewThe Journal of physiology2016

Sympathetic-mediated activation versus suppression of the immune system: consequences for hypertension.

Adam J Case, Matthew C Zimmerman

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Hypertension and its management in COVID-19 patients: The assorted view.International journal of cardiology. Cardiovascular risk and prevention · 2021
    Review
  9. Observational
  10. Article
  11. Cardiometabolic risk factors are associated with immune cell mitochondrial respiration in humans.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  12. Review
  13. Review
  14. Immune mechanisms of hypertension.Nature reviews. Immunology · 2019
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Loneliness, Social Isolation, and Cardiovascular Health.Antioxidants & redox signaling · 2018
    Review
  20. Review
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

2 authors at 1 institution in 1 country.

Adam J CaseDepartment of Cellular and Integrative Physiology, University of Nebraska Medical Centre, Omaha, NE, USA.
Matthew C ZimmermanDepartment of Cellular and Integrative Physiology, University of Nebraska Medical Centre, Omaha, NE, USA.
University of Nebraska Medical Center · US

Funding

TRAINING PROGRAM IN FREE RADICAL AND RADIATION BIOLOGYT32CA078586 · NCI · UNIVERSITY OF IOWA · PI SPITZ, DOUGLAS ROBERT · 1999 to 2024
$5.7M
Mitochondrial Redox Systems in Neurogenic HypertensionR01HL103942 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI ZIMMERMAN, MATTHEW C. · 2010 to 2014
$1.8M
Redox Regulation of T-lymphocytes in Sympathoexcitation-associated HypertensionR00HL123471 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI CASE, ADAM J · 2016 to 2018
$765k
Redox Regulation of T-lymphocytes in Sympathoexcitation-associated HypertensionK99HL123471 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI CASE, ADAM J · 2015 to 2015
$108k
NCI NIH HHS T32 CA078586NHLBI NIH HHS K99 HL123471NHLBI NIH HHS R00 HL123471NHLBI NIH HHS R01 HL103942
6 · The paper itself

Abstract

It is generally well-accepted that the immune system is a significant contributor in the pathogenesis of hypertension. Specifically, activated and pro-inflammatory T-lymphocytes located primarily in the vasculature and kidneys appear to have a causal role in exacerbating elevated blood pressure. It has been proposed that increased sympathetic nerve activity and noradrenaline outflow associated with hypertension may be primary contributors to the initial activation of the immune system early in the disease progression. However, it has been repeatedly demonstrated in many different human and experimental diseases that sympathoexcitation is immunosuppressive in nature. Moreover, human hypertensive patients have demonstrated increased susceptibility to secondary immune insults like infections. Thus, it is plausible, and perhaps even likely, that in diseases like hypertension, specific immune cells are activated by increased noradrenaline, while others are in fact suppressed. We propose a model in which this differential regulation is based upon activation status of the immune cell as well as the resident organ. With this, the concept of global immunosuppression is obfuscated as a viable target for hypertension treatment, and we put forth the concept of focused organ-specific immunotherapy as an alternative option.

Indexed as

HypertensionSympathetic Nervous SystemT-LymphocytesAnimalsHumans

Identifiers

PMID26830047
PMCPMC4930069
OpenAlexW2179644821

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.