Evidence map›Paper›PMID 37920479›Full record

ArticleJVS-vascular science2023

Vascular smooth muscle cell mechanotransduction through serum and glucocorticoid inducible kinase-1 promotes interleukin-6 production and macrophage accumulation in murine hypertension.

Mario Figueroa, SarahRose Hall, Victoria Mattia, Alex Mendoza, Adam Brown, Ying Xiong, Rupak Mukherjee, Jeffrey A Jones, William Richardson, Jean Marie Ruddy

Open access · goldAbstract read
In one paragraph

Article in JVS-vascular science, 2023. 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
0.8field-weighted citation impact, top 25% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
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  5. 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

10 authors at 2 institutions in 1 country.

Mario FigueroaDivision of Vascular Surgery, Medical University of South Carolina, Charleston, SC.
SarahRose HallDivision of Vascular Surgery, Medical University of South Carolina, Charleston, SC.
Victoria MattiaDivision of Vascular Surgery, Medical University of South Carolina, Charleston, SC.
Alex MendozaDivision of Vascular Surgery, Medical University of South Carolina, Charleston, SC.
Adam BrownDivision of Vascular Surgery, Medical University of South Carolina, Charleston, SC.
Ying XiongDivision of Cardiothoracic Surgery, Medical University of South Carolina, Charleston, SC.
Rupak MukherjeeDivision of Cardiothoracic Surgery, Medical University of South Carolina, Charleston, SC.
Jeffrey A JonesDivision of Cardiothoracic Surgery, Medical University of South Carolina, Charleston, SC.
William RichardsonDepartment of Chemical Engineering, University of Arkansas, Fayetteville, AK.
Jean Marie RuddyDivision of Vascular Surgery, Medical University of South Carolina, Charleston, SC.
Medical University of South Carolina · USUniversity of Arkansas at Fayetteville · US

Funding

Training Grant in Inflammatory and Fibrosing DiseasesT32AR050958 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI DIANE L KAMEN · 2005 to 2026
$4.2M
Systems Mechanobiology Modeling for Patient-Specific Cardiac Fibrosis PredictionsR01HL144927 · NHLBI · UNIVERSITY OF ARKANSAS AT FAYETTEVILLE · PI RICHARDSON, WILLIAM JAMES · 2019 to 2023
$1.8M
Tension-induced SGK-1 Signaling in AAAK08HL143169 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RUDDY, JEAN MARIE · 2019 to 2023
$882k
BLRD VA I01 BX000904NHLBI NIH HHS K08 HL143169NHLBI NIH HHS R01 HL144927NIAMS NIH HHS T32 AR050958
6 · The paper itself

Abstract

Objective: The objective of this investigation was to demonstrate that in vivo induction of hypertension (HTN) and in vitro cyclic stretch of aortic vascular smooth muscle cells (VSMCs) can cause serum and glucocorticoid-inducible kinase (SGK-1)-dependent production of cytokines to promote macrophage accumulation that may promote vascular pathology. Methods: HTN was induced in C57Bl/6 mice with angiotensin II infusion (1.46 mg/kg/day × 21 days) with or without systemic infusion of EMD638683 (2.5 mg/kg/day × 21 days), a selective SGK-1 inhibitor. Systolic blood pressure was recorded. Abdominal aortas were harvested to quantify SGK-1 activity (pSGK-1/SGK-1) by immunoblot. Flow cytometry quantified the abundance of CD11b Results: SGK-1 activity, abundance of CD11b Conclusions: Mechanical activation of SGK-1 in aortic VSMCs can promote inflammatory signaling and increased macrophage abundance, therefore this kinase warrants further exploration as a pharmacotherapeutic target to abrogate hypertensive vascular pathology.

Indexed as

HypertensionInterleukin-6Serum and glucocorticoid-inducible kinase-1 (SGK-1)

Identifiers

PMID37920479
PMCPMC10618507
OpenAlexW4385728250

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.