Evidence mapPaperPMID 39150393Full record

SynthesisAmerican journal of physiology. Heart and circulatory physiology2024

Effects of excess sodium consumption on arterial function in C57BL/6 mice.

Mostafa Sabouri, Xiangyu Zheng, Bryan J Irwin, Daniel R Machin

Abstract readMeta-Analysis
In one paragraph

Synthesis in American journal of physiology. Heart and circulatory physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

4 authors.

Mostafa SabouriVascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico, United States.
Xiangyu ZhengDepartment of Nutrition and Integrative Physiology, Florida State University, Tallahassee, Florida, United States.ORCID 0000-0002-1761-2172
Bryan J IrwinDepartment of Biological Science, Florida State University, Tallahassee, Florida, United States.
Daniel R MachinVascular Physiology Group, Department of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico, United States.ORCID 0000-0002-2509-4686

Funding

NCCIH NIH HHS K99 AT010017NCCIH NIH HHS R00 AT010017NIAMS NIH HHS L30 AR070535
6 · The paper itself

Abstract

Excess sodium consumption contributes to arterial dysfunction in humans. The C57BL/6 strain of mice has been used to identify mechanisms by which arterial dysfunction occurs after excess sodium consumption. However, there are concerns that C57BL/6 mice have strain-specific resistance to high-sodium (HS) diet-induced hypertension. To address this concern, we performed a meta-analysis to determine if excess sodium consumption in C57BL/6 mice induces arterial dysfunction. Databases were searched for HS versus standard diet studies that measured arterial function [i.e., systolic blood pressure (BP), endothelium-dependent dilation (EDD), and central arterial stiffness] in C57BL/6 mice. A total of 39 studies were included, demonstrating that the HS condition resulted in higher systolic BP than control mice with a mean difference of 9.8 mmHg (95% confidence interval [CI] = [5.6, 14],

Indexed as

Mice, Inbred C57BLSodium, DietaryVascular StiffnessAnimalsArteriesBlood PressureDisease Models, AnimalEndothelium, VascularHypertensionMiceVasodilationSodium, Dietaryarterial stiffnessblood pressureendothelial functioninbred micesalt

Identifiers

PMID39150393
PMCPMC11482244

What Socratic 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 Socratic graph.