Evidence map›Paper›PMID 28453726›Full record

ArticleCardiovascular research2017

Osteopontin RNA aptamer can prevent and reverse pressure overload-induced heart failure.

Jihe Li, Keyvan Yousefi, Wen Ding, Jayanti Singh, Lina A Shehadeh

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Recent Advances in Aptamer-Based Applications in Cardiology.International journal of molecular sciences · 2026
    Review
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  19. Silencing Survivin: a Key Therapeutic Strategy for Cardiac Hypertrophy.Journal of cardiovascular translational research · 2022
    Article
  20. The Role of Matrix Proteins in Cardiac Pathology.International journal of molecular sciences · 2022
    Review
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

5 authors at 1 institution in 1 country.

Jihe LiDepartment of Medicine, Division of Cardiology, University of Miami Leonard M. Miller School of Medicine, Miami, FL 33136, USA.
Keyvan YousefiInterdisciplinary Stem Cell Institute, University of Miami Leonard M. Miller School of Medicine, Biomedical Research Building, Room 818, 1501 NW 10th Avenue, Miami, FL 33136, USA.
Wen DingInterdisciplinary Stem Cell Institute, University of Miami Leonard M. Miller School of Medicine, Biomedical Research Building, Room 818, 1501 NW 10th Avenue, Miami, FL 33136, USA.
Jayanti SinghDepartment of Medicine, Division of Cardiology, University of Miami Leonard M. Miller School of Medicine, Miami, FL 33136, USA.
Lina A ShehadehDepartment of Medicine, Division of Cardiology, University of Miami Leonard M. Miller School of Medicine, Miami, FL 33136, USA.
University of Miami · US

Funding

Mechanisms for miR-30e Regulated Atherogenic Pathways with AgeK01AG040468 · NIA · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SHEHADEH, LINA A · 2012 to 2014
$365k
NIA NIH HHS K01 AG040468
6 · The paper itself

Abstract

aimsCardiac myocyte hypertrophy, the main compensatory response to chronic stress in the heart often progresses to a state of decompensation that can lead to heart failure. Osteopontin (OPN) is an effector for extracellular signalling that induces myocyte growth and fibrosis. Although increased OPN activity has been observed in stressed myocytes and fibroblasts, the detailed and long term effects of blocking OPN signalling on the heart remain poorly defined. Targeting cardiac OPN protein by an RNA aptamer may be beneficial for tuning down OPN pathologic signalling. We aimed to demonstrate the therapeutic effects of an OPN RNA aptamer on cardiac dysfunction. METHODS AND

resultsIn vivo, we show that in a mouse model of pressure overload, treating at the time of surgeries with an OPN aptamer prevented cardiomyocyte hypertrophy and cardiac fibrosis, blocked OPN downstream signalling (PI3K and Akt phosphorylation), reduced expression of extracellular matrix (Lum, Col3a1, Fn1) and hypertrophy (Nppa, Nppb) genes, and prevented cardiac dysfunction. Treating at two months post-surgeries with the OPN aptamer reversed cardiac dysfunction and fibrosis and myocyte hypertrophy. While genetic homozygous deletion of OPN reduced myocardial wall thickness, surprisingly cardiac function and myocardial fibrosis, specifically collagen deposition and myofibroblast infiltration, were worse compared with wild type mice at three months of pressure overload.

conclusionTaken together, these data demonstrate that tuning down cardiac OPN signalling by an OPN RNA aptamer is a novel and effective approach for preventing cardiac hypertrophy and fibrosis, improving cardiac function, and reversing pressure overload-induced heart failure.

Indexed as

Arterial PressureVentricular Function, LeftVentricular RemodelingAnimalsAortaAptamers, NucleotideCollagen Type IIICytokinesDisease Models, AnimalFibrosisGene Expression RegulationGenetic Predisposition to DiseaseHeart FailureHypertrophy, Left VentricularLigationLumicanAptamers, NucleotideCOL3A1 protein, mouseCollagen Type IIICytokinesLumicanLum protein, mouseOsteopontinPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktSpp1 protein, mouseAptamerCardiac fibrosisCardiac hypertrophyHeart failureOsteopontinTAC

Identifiers

PMID28453726
PMCPMC7526752
OpenAlexW2584978057

What OpenQuestion 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 OpenQuestion graph.