Evidence map›Paper›PMID 40144661›Full record

ReviewFrontiers in pharmacology2025

Salt-sensitive hypertension: role of endothelial and vascular dysfunction and sex.

Helen M Butler, Marice K McCrorey, Lada Palygina, Ryan Lacey, Justin P Van Beusecum

Abstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. 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

5 authors.

Helen M ButlerDivision of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, SC, United States.
Marice K McCroreyDivision of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, SC, United States.
Lada PalyginaDivision of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, SC, United States.
Ryan LaceyDivision of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, SC, United States.
Justin P Van BeusecumDivision of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, SC, United States.

Funding

MUSC IMSDT32GM152386 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI ERGUL, ADVIYE, RINKER, JENNIFER ANNE · 2024 to 2024
$460k
BLRD VA IK2 BX005605NIGMS NIH HHS T32 GM152386
6 · The paper itself

Abstract

For the last 120 years, the contribution of salt has been identified in the pathophysiological elevation of blood pressure. Since then, both human and experimental murine studies have begun to elucidate the key mechanisms contributing to the development of salt-sensitive hypertension. Numerous mechanisms, including increased plasma volume, sodium retention, impaired autoregulatory capability, inflammation, and endothelial and vascular dysfunction, contribute to deleterious elevations in blood pressure during salt sensitivity. The endothelium plays a critical role in blood flow regulation, renal blood flow, and blood pressure elevations and in migrating immune cells to end-organs, contributing to end-organ damage and fibrosis. In this review, we will consider the clinical studies setting the foundation for the definition of salt-sensitive hypertension, murine models to study endothelial and vascular contributions, and endothelial cell cultures that have shed light on signaling mechanisms. Lastly, we will discuss the sex-dependent physiology and mechanisms contributing to salt-sensitive hypertension development and their clinical implications.

Indexed as

endothelial cell (EC)endothelial dysfunctionsalt-sensitive blood pressuresex differencesvascular

Identifiers

PMID40144661
PMCPMC11936959

What OpenQuestion holds

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Registered trials

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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.