Evidence map›Paper›PMID 30319717›Full record

ArticleCellular and molecular bioengineering2017

Shape-Specific Nanoceria Mitigate Oxidative Stress-Induced Calcification in Primary Human Valvular Interstitial Cell Culture.

Yingfei Xue, Cynthia St Hilaire, Luis Hortells, Julie A Phillippi, Vinayak Sant, Shilpa Sant

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular bioengineering, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.5field-weighted citation impact, top 41% 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

6 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. 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

6 authors at 2 institutions in 1 country.

Yingfei XueDepartment of Pharmaceutical Sciences, University of Pittsburgh School of Pharmacy, Pittsburgh, PA 15261, USA.
Cynthia St HilaireDepartment of Medicine, Division of Cardiology & Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, PA 15219, USA.
Luis HortellsDepartment of Medicine, Division of Cardiology & Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, PA 15219, USA.
Julie A PhillippiDepartment of Bioengineering, University of Pittsburgh Swanson School of Engineering, Pittsburgh, PA 15261, USA.
Vinayak SantDepartment of Pharmaceutical Sciences, University of Pittsburgh School of Pharmacy, Pittsburgh, PA 15261, USA.
Shilpa SantDepartment of Pharmaceutical Sciences, University of Pittsburgh School of Pharmacy, Pittsburgh, PA 15261, USA.
University of Pittsburgh · USSalk Institute for Biological Studies · US

Funding

Regulation of Vascular Calcification by Adenosine SignalingK22HL117917 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ST. HILAIRE, CYNTHIA · 2015 to 2017
$731k
NHLBI NIH HHS K22 HL117917
6 · The paper itself

Abstract

introductionLack of effective pharmacological treatment makes valvular calcification a significant clinical problem in patients with valvular disease and bioprosthetic/mechanical valve replacement therapies. Elevated levels of reactive oxygen species (ROS) in valve tissue have been identified as a prominent hallmark and driving factor for valvular calcification. However, the therapeutic value of ROS-modulating agents for valvular calcification remains elusive. We hypothesized that ROS-modulating shape-specific cerium oxide nanoparticles (CNPs) will inhibit oxidative stress-induced valvular calcification. CNPs are a class of self-regenerative ROS-modulating agents, which can switch between Ce

methodsHuman valvular interstitial cells (hVICs) were obtained from a normal healthy donor and two patients with calcified aortic valves. hVICs were characterized for their phenotypic (mesenchymal, myofibroblast and osteoblast) marker expression by qRT-PCR and antioxidant enzymes activity before and after exposure to hydrogen peroxide (H

resultshVICs isolated from calcified valves exhibited elevated osteoblast marker expression and decreased antioxidant enzyme activities compared to the normal hVICs. Due to the impaired antioxidant enzyme activities, acute H

conclusionsWe demonstrated that hVICs derived from calcified valves exhibited impaired antioxidant defense mechanisms and were more susceptible to oxidative stress than normal hVICs. CNPs scavenged H

Indexed as

Cerium oxide nanoparticleNanoceriaNanoparticle shapePatient-derived valvular interstitial cells (hVICs)Reactive oxygen species (ROS)Valve calcification

Identifiers

PMID30319717
PMCPMC6178984
OpenAlexW2736319201

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.