Evidence map›Paper›PMID 30377822›Full record

ReviewCurrent hypertension reports2018

Inflammation in Salt-Sensitive Hypertension and Renal Damage.

Xiaohan Lu, Steven D Crowley

Open access · greenAbstract readReview
In one paragraph

Review in Current hypertension reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

58 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Network pharmacology andArchives of medical science : AMS · 2026
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Immunology of Hypertension: Pathophysiological and Therapeutic Aspects.International journal of molecular sciences · 2025
    Review
  11. Article
  12. Article
  13. HMGB1 drives T-cell activation in hypertensive males and females.American journal of physiology. Renal physiology · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. The roles of G protein-coupled receptor kinase 2 in renal diseases.Journal of cellular and molecular medicine · 2024
    Review
  18. Perspectives on the involvement of the gut microbiota in salt-sensitive hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Review
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Xiaohan LuDivision of Nephrology, Department of Medicine, Duke University and Durham VA Medical Centers, Durham, NC, 27710, USA.
Steven D CrowleyDivision of Nephrology, Department of Medicine, Duke University and Durham VA Medical Centers, Durham, NC, 27710, USA. steven.d.crowley@duke.edu.
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
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 interleukin-1 receptor regulates crosstalk between myeloid and renal tubular cells in hypertensionR01DK118019 · NIDDK · DUKE UNIVERSITY · PI CROWLEY, STEVEN D · 2019 to 2022
$1.7M
BLRD VA I01 BX000893NHLBI NIH HHS R01 HL128355NIDDK NIH HHS R01 DK087893NIDDK NIH HHS R01 DK118019
6 · The paper itself

Abstract

purpose of reviewLow-grade inflammation drives elevations in blood pressure (BP) and consequent target organ damage in diverse experimental models of hypertension. Here, we discuss recent advances elucidating immune-mediated mechanisms of BP elevation and associated target organ damage. RECENT

findingsInflammatory mediators produced by immune cells or target organs act on the kidney, vasculature, skin, and nervous system to modulate hypertension. For example, cells of the innate immune system, including monocytes, neutrophils, and dendritic cells (DCs), can all promote BP elevation via actions in the vasculature and kidney. Macrophages expressing VEGF-C impact non-osmotic sodium storage in the skin that in turn regulates salt sensitivity. Within the adaptive immune system, activated T cells can secrete tumor necrosis factor-alpha (TNF-α), interleukin-17a (IL-17a), and interferon-gamma (IFN-γ), each of which has augmented BP and renal damage in pre-clinical models. Inversely, deficiency of IL-17a in mice blunts the hypertensive response and attenuates renal sodium retention via a serum- and glucocorticoid-regulated kinase 1 (SGK1)-dependent pathway. Linking innate and adaptive immune responses, dendritic cells activated by augmented extracellular sodium concentrations stimulate T lymphocytes to produce pro-hypertensive cytokines. By contrast, regulatory T cells (Tregs) can protect against hypertension and associated kidney injury. Rodent studies reveal diverse mechanisms via which cells of the innate and adaptive immune systems drive blood pressure elevation by altering the inflammatory milieu in the kidney, vasculature, and brain.

Indexed as

HypertensionKidneyAnimalsBlood PressureHumansInflammationMiceSodium ChlorideSodium ChlorideCytokinesHypertensionImmunityInflammationRenal damage

Identifiers

PMID30377822
PMCPMC8059874
OpenAlexW2899205995

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.