Evidence map›Paper›PMID 30527626›Full record

ReviewEBioMedicine2019

Mineralocorticoid receptor: A hidden culprit for hemodialysis vascular access dysfunction.

Bohan Chen, Pei Wang, Andrew Brem, Lance Dworkin, Zhangsuo Liu, Rujun Gong

Open access · goldAbstract readReview
In one paragraph

Review in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.8field-weighted citation impact, top 24% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Mineralocorticoid receptor antagonism attenuates arteriovenous fistula stenosis by modulating the phenotype of vascular smooth muscle cells.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025
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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

6 authors at 3 institutions in 2 countries.

Bohan ChenInstitute of Nephrology, Blood Purification Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China; Division of Kidney Disease and Hypertension, Department of Medicine, Brown University School of Medicine, Providence, RI, United States; Division of Nephrology, Department of Medicine, University of Toledo College of Medicine, Toledo, OH, United States.
Pei WangInstitute of Nephrology, Blood Purification Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Andrew BremDivision of Kidney Disease and Hypertension, Department of Medicine, Brown University School of Medicine, Providence, RI, United States.
Lance DworkinDivision of Nephrology, Department of Medicine, University of Toledo College of Medicine, Toledo, OH, United States.
Zhangsuo LiuInstitute of Nephrology, Blood Purification Center, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, China. Electronic address: zhangsuoliu@zzu.edu.cn.
Rujun GongDivision of Kidney Disease and Hypertension, Department of Medicine, Brown University School of Medicine, Providence, RI, United States; Division of Nephrology, Department of Medicine, University of Toledo College of Medicine, Toledo, OH, United States. Electronic address: Rujun.Gong@UToledo.edu.
First Affiliated Hospital of Zhengzhou University · CNBrown University · USUniversity of Toledo · US

Funding

Therapeutic targeting of GSK3beta: A novel approach for podocyte protectionR01DK092485 · NIDDK · RHODE ISLAND HOSPITAL · PI GONG, RUJUN · 2011 to 2015
$1.8M
The Melanocortinergic pathway inglomerular diseaseR01DK114006 · NIDDK · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI GONG, RUJUN · 2017 to 2021
$1.8M
NIDDK NIH HHS R01 DK092485NIDDK NIH HHS R01 DK114006
6 · The paper itself

Abstract

Hemodialysis vascular access dysfunction is a common and intractable problem in clinical practice with no definitive therapy yet available. As a key mediator of vascular and cardiac maladaptive remodeling, mineralocorticoid receptor (MR) plays a pivotal role in vascular fibrosis and intimal hyperplasia (IH) and is potentiated locally in hemodialysis vascular access following diverse injuries, like barotrauma, cannulation and shear stress. MR-related genomic and non-genomic pathways are responsible for triggering vascular smooth muscle cell activation, proliferation, migration and extracellular matrix overproduction. In endothelial cells, MR signaling diminishes nitric oxide production and its bioavailability, but amplifies reactive oxygen species, leading to an inflammatory state. Moreover, MR favors macrophage polarization towards a pro-inflammatory phenotype. In clinical settings like post-angioplasty or stenting restenosis, the beneficial effect of MR antagonists on vascular fibrosis and IH has been validated. In aggregate, therapeutic targeting of MR may provide a new avenue to prevent hemodialysis vascular access dysfunction.

Indexed as

Cell MovementCell ProliferationFibrosisHumansHyperplasiaMuscle, Smooth, VascularMyocytes, Smooth MuscleNitric OxideReactive Oxygen SpeciesReceptors, MineralocorticoidRenal DialysisSignal TransductionTunica IntimaNitric OxideReactive Oxygen SpeciesReceptors, MineralocorticoidAldosteroneArteriovenous fistula failureHemodialysis vascular access dysfunctionIntimal hyperplasiaMineralocorticoid receptor

Identifiers

PMID30527626
PMCPMC6354623
OpenAlexW2903336022

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.