Evidence map›Paper›PMID 29140820›Full record

ReviewCurrent opinion in nephrology and hypertension2018

Renal effects of cytokines in hypertension.

Yi Wen, Steven D Crowley

Abstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Immunology of Hypertension: Pathophysiological and Therapeutic Aspects.International journal of molecular sciences · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
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  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Current Understanding of Pressure Natriuresis.Electrolyte & blood pressure : E & BP · 2021
    Review
  20. Molecular Interactions of Arterial Hypertension in Its Target Organs.International journal of molecular sciences · 2021
    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 2 institutions in 2 countries.

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

Funding

Renal Genomics CoreP30DK096493 · NIDDK · DUKE UNIVERSITY · PI COFFMAN, THOMAS M · 2012 to 2016
$5.9M
Role of Th1 Immune Responses in the Pathogenesis of Hypertensive Kidney InjuryR01DK087893 · NIDDK · DUKE UNIVERSITY · PI CROWLEY, STEVEN D · 2010 to 2018
$2.4M
Role of Dendritic Cell-mediated T Cell Activation in Salt-sensitive HypertensionR01HL128355 · NHLBI · DUKE UNIVERSITY · PI CROWLEY, STEVEN D · 2016 to 2019
$1.9M
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 BX000893NHLBI NIH HHS R01 HL128355NIDDK NIH HHS P30 DK096493NIDDK NIH HHS R01 DK087893
6 · The paper itself

Abstract

purpose of reviewInflammatory cytokines contribute to the pathogenesis of hypertension through effects on renal blood flow and sodium handling. This review will update recent advances that explore the renal actions of immune cells and cytokines in the pathogenesis of hypertension. RECENT

findingsPopulations of cells from both the innate and adaptive immune systems contribute to hypertension by modulating functions of the vasculature and epithelial cells in the kidney. Macrophages and T lymphocytes can directly regulate the hypertensive response and consequent target organ damage. Dendritic cells and B lymphocytes can alter blood pressure (BP) indirectly by facilitating T-cell activation. Proinflammatory cytokines, including tumor necrosis factor-α, interleukin 17, interleukin 1, and interferon-γ augment BP and/or renal injury when produced by T helper 1 cells, T helper 17 cells, and macrophages. In contrast, interleukin 10 improves vascular and renal functions in preclinical hypertension studies. The effects of transforming growth factor-β are complex because of its profibrotic and immunosuppressive functions that also depend on the localization and concentration of this pleiotropic cytokine. SUMMARY: Preclinical studies point to a key role for cytokines in hypertension via their actions in the kidney. Consistent with this notion, anti-inflammatory therapies can attenuate BP elevation in human patients with rheumatologic disease. Conversely, impaired natriuresis may further polarize both T lymphocytes and macrophages toward a proinflammatory state, in a pathogenic, feed-forward loop of immune activation and BP elevation. Understanding the precise renal actions of cytokines in hypertension will be necessary to inhibit cytokine-dependent hypertensive responses while preserving systemic immunity and tumor surveillance.

Indexed as

B-LymphocytesCytokinesDendritic CellsHumansHypertensionKidneyLymphocyte ActivationMacrophagesT-LymphocytesCytokines

Identifiers

PMID29140820
PMCPMC5792304
OpenAlexW2768855251

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.