Evidence map›Paper›PMID 40229965›Full record

ArticleAdvanced biology2025

PTEN Regulates Myofibroblast Activation in Valvular Interstitial Cells Based on Subcellular Localization.

Dilara Batan, Georgios Tseropoulos, Bruce E Kirkpatrick, Carrie Bishop, Kaustav Bera, Alex Khang, Mary Weiser-Evans, Kristi S Anseth

Abstract read
In one paragraph

Article in Advanced biology, 2025. 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. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Dilara BatanDepartment of Chemical and Biological Engineering, University of Colorado, Boulder, Colorado, 80303, USA.
Georgios TseropoulosDepartment of Chemical and Biological Engineering, University of Colorado, Boulder, Colorado, 80303, USA.
Bruce E KirkpatrickDepartment of Chemical and Biological Engineering, University of Colorado, Boulder, Colorado, 80303, USA.
Carrie BishopDepartment of Chemical and Biological Engineering, University of Colorado, Boulder, Colorado, 80303, USA.
Kaustav BeraDepartment of Chemical and Biological Engineering, University of Colorado, Boulder, Colorado, 80303, USA.
Alex KhangDepartment of Chemical and Biological Engineering, University of Colorado, Boulder, Colorado, 80303, USA.
Mary Weiser-EvansDepartment of Medicine, Division of Renal Diseases and Hypertension, University of Colorado, Anschutz Medical Campus, 12700 East 19th Avenue, C281, Research Complex 2, Room 7101, Aurora, Colorado, 80045, USA.
Kristi S AnsethDepartment of Chemical and Biological Engineering, University of Colorado, Boulder, Colorado, 80303, USA.ORCID https://orcid.org/0000-0002-5725-5691

Funding

POSTGRADUATE TRAINING IN CARDIOVASCULAR RESEARCHT32HL007822 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI BUTTRICK, PETER N., LEINWAND, LESLIE ANNE · 1996 to 2023
$6.2M
Propagation and Resolution of Injury in Calcific Aortic Valve DiseaseR01HL142935 · NHLBI · UNIVERSITY OF IOWA · PI WEISS, ROBERT M · 2018 to 2022
$2.3M
Hydrogel matrices to study the role of inflammation and biological sex on aortic valve fibrocalcificationR01HL171197 · NHLBI · UNIVERSITY OF COLORADO · PI KRISTI S. ANSETH, ROBERT M WEISS · 2024 to 2026
$2.0M
Hydrogels to Study Synergistic Effects of Signaling Factors and Matrix Mechanics on Valve Disease ProgressionR01HL132353 · NHLBI · UNIVERSITY OF COLORADO · PI ANSETH, KRISTI S. · 2017 to 2020
$1.4M
Identifying the Role of Fibroblast-Macrophage Crosstalk in Aortic Valve Stenosis Sexual DimorphismF32HL176073 · NHLBI · UNIVERSITY OF COLORADO · PI KHANG, ALEX · 2024 to 2024
$74k
American Heart Association 20PRE35200068Helen Hay Whitney Foundation F1339NHLBI NIH HHS F32 HL176073NHLBI NIH HHS R01 HL132353NHLBI NIH HHS R01 HL142935NHLBI NIH HHS R01 HL171197NHLBI NIH HHS T32 HL007822NIH HHS R01 HL132353NIH HHS R01 HL142935NIH HHS T32 HL007822
6 · The paper itself

Abstract

Aortic valve stenosis (AVS) is characterized by altered mechanics of the valve leaflets, which disrupts blood flow through the aorta and can cause left ventricle hypotrophy. These changes in the valve tissue result in the activation of resident valvular interstitial cells (VICs) into myofibroblasts, which have increased levels of αSMA in their stress fibers. The persistence of VIC myofibroblast activation is a hallmark of AVS. In recent years, the tumor suppressor gene phosphatase and tensin homolog (PTEN) has emerged as an important player in the regulation of fibrosis in various tissues (e.g., lung, skin), which motivated to investigate PTEN as a potential protective factor against matrix-induced myofibroblast activation in VICs. In aortic valve samples from humans, high levels of PTEN are found in healthy tissue and low levels of PTEN in diseased tissue. Then, using pharmacological inducers to treat VIC cultures, it is observed that PTEN overexpression prevented stiffness-induced myofibroblast activation, whereas genetic and pharmacological inhibition of PTEN further activated myofibroblasts. The increased nuclear PTEN localization is also observed in VICs cultured on stiff matrices, and nuclear PTEN also correlated with smaller nuclei, altered expression of histones, and a quiescent fibroblast phenotype. Together, these results suggest that PTEN not only suppresses VIC activation, but functions to promote quiescence, and can serve as a potential pharmacological target for the treatment of AVS.

Indexed as

Aortic ValveAortic Valve StenosisMyofibroblastsPTEN PhosphohydrolaseCells, CulturedHumansPTEN PhosphohydrolasePTEN protein, humanfibrosisheart valvehydrogelsinterstitial cells

Identifiers

PMID40229965
PMCPMC12266975

What Socratic 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 Socratic graph.