Evidence map›Paper›PMID 23472597›Full record

ReviewAntioxidants & redox signaling2014

The cooperative roles of inflammation and oxidative stress in the pathogenesis of hypertension.

Steven D Crowley

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 2 pooled it
9.7field-weighted citation impact, top 1% 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

86 citing papers in PubMed, 2 syntheses or guidelines pooled it, 188 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. The association between pro-inflammatory diet and incidence of hypertension: a prospective cohort study.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
    Article
  6. Review
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  10. Observational
  11. Review
  12. [Mediating role of insulin resistance in the relationship between hypertension and NAFLD and construction of its risk prediction model].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
    Article
  13. Markers of Vascular Dysfunction in Hypertension.Current medicinal chemistry · 2025
    Review
  14. Article
  15. Synergistic Effect of the CHATherapeutics and clinical risk management · 2025
    Article
  16. Article
  17. Review
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  20. Article

26 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

1 author at 1 institution in 1 country.

Steven D CrowleyDivision of Nephrology, Department of Medicine, Duke University and Durham VA Medical Centers , Durham, North Carolina.
Duke University · US

Funding

Role of Th1 Immune Responses in the Pathogenesis of Hypertensive Kidney InjuryR01DK087893 · NIDDK · DUKE UNIVERSITY · PI CROWLEY, STEVEN D · 2010 to 2018
$2.4M
Alkali Therapy in Chronic Kidney DiseaseU01DK087783 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI HOSTETTER, THOMAS HEARD · 2013 to 2015
$1.1M
Alkali Therapy in Chronic Kidney DiseaseR01DK087783 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI HOSTETTER, THOMAS HEARD · 2010 to 2012
$750k
The role of the M1 macrophage response in the progression of chronic kidney diseaseI01BX000893 · VA · DURHAM VA MEDICAL CENTER · PI Steven D Crowley · 2012 to 2026
–
BLRD VA I01 BX000893NIDDK NIH HHS DK087783NIDDK NIH HHS R01 DK087893
6 · The paper itself

Abstract

significanceInnate and adaptive immunity play fundamental roles in the development of hypertension and its complications. As effectors of the cell-mediated immune response, myeloid cells and T lymphocytes protect the host organism from infection by attacking foreign intruders with bursts of reactive oxygen species (ROS). RECENT ADVANCES: While these ROS may help to preserve the vascular tone and thereby protect against circulatory collapse in the face of overwhelming infection, aberrant elaboration of ROS triggered by immune cells in the absence of a hemodynamic insult can lead to pathologic increases in blood pressure. Conversely, misdirected oxidative stress in cardiovascular control organs, including the vasculature, the kidney, and the nervous system potentiates inflammatory responses, augmenting blood pressure elevation and inciting target organ damage. CRITICAL ISSUES: Inflammation and oxidative stress thereby act as cooperative and synergistic partners in the pathogenesis of hypertension. FUTURE DIRECTIONS: Pharmacologic interventions for hypertensive patients will need to exploit this robust bidirectional relationship between ROS generation and immune activation in cardiovascular control organs to maximize therapeutic benefit, while limiting off-target side effects.

Indexed as

Oxidative StressAnimalsCardiovascular SystemHumansHypertensionInflammationReactive Oxygen SpeciesReactive Oxygen Species

Identifiers

PMID23472597
PMCPMC3880899
OpenAlexW2312275660

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.