ArticleCardiovascular research2010
Influence of p53 in the transition of myotrophin-induced cardiac hypertrophy to heart failure.
Article in Cardiovascular research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 papers.
What it found
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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.
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.
Who cites it
13 citing papers in PubMed, 37 citations in OpenAlex.
- Exploring novel biomarkers in dilated cardiomyopathy‑induced heart failure by integrated analysis andExperimental and therapeutic medicine · 2023Article
- Untargeted sequencing of circulating microRNAs in a healthy and diseased older population.Scientific reports · 2022Article
- Runt-related transcription factor 1 (Runx1) aggravates pathological cardiac hypertrophy by promoting p53 expression.Journal of cellular and molecular medicine · 2021Article
- Platelet proteome changes in dogs with congestive heart failure.BMC veterinary research · 2020Article
- Identification of transcription factors MYC and C/EBPβ mediated regulatory networks in heart failure based on gene expression omnibus datasets.BMC cardiovascular disorders · 2020Article
- Overexpression of peptidase inhibitor 16 attenuates angiotensin II-induced cardiac fibrosis via regulating HDAC1 of cardiac fibroblasts.Journal of cellular and molecular medicine · 2020Article
- Excision of the expanded GAA repeats corrects cardiomyopathy phenotypes of iPSC-derived Friedreich's ataxia cardiomyocytes.Stem cell research · 2019Article
- Association of Parkinson Disease Induction with Cardiac Upregulation of Apoptotic Mediators P53 and Active Caspase-3: An Immunohistochemistry Study.Medical science monitor basic research · 2018Article
- V-1 regulates capping protein activity in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- miR-30c and miR-181a synergistically modulate p53-p21 pathway in diabetes induced cardiac hypertrophy.Molecular and cellular biochemistry · 2016Article
- Tanshinone IIA inhibits apoptosis in the myocardium by inducing microRNA-152-3p expression and thereby downregulating PTEN.American journal of translational research · 2016Article
- Class III PI3K-mediated prolonged activation of autophagy plays a critical role in the transition of cardiac hypertrophy to heart failure.Journal of cellular and molecular medicine · 2015Article
- Safflower extract inhibiting apoptosis by inducing autophagy in myocardium derived H9C2 cell.International journal of clinical and experimental medicine · 2015Article
Corrections and comments
- Expression of concern · 2021-01-22Concerns/Issues about Image · Investigation by Company/Institution · Objections by Third Party · Updated to Retraction ·
- Retraction · 2021-04-22Concerns/Issues about Data · Investigation by Company/Institution · Original Data and/or Images not Provided and/or not Available · Upgrade/Update of Prior Notice(s) ·
- Expression of concern
- Retracted
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
aimsCardiac-specific overexpression of myotrophin (myo) protein in transgenic (myo-Tg) mice results in hypertrophy at 4 weeks that progresses to heart failure (HF) by 36 weeks. Gene profiling showed that p53 expression increases as hypertrophy worsens to HF, suggesting that p53 may influence myo-induced HF. We aimed to define how the p53 signalling cascade affects the spectrum of cardiac hypertrophy (CH)/HF. METHODS AND
resultsImmunoblot analysis showed that in myo-Tg mice (Mus musculus), upregulation of p53 occurs only when hypertrophy transitions to HF (16 weeks onward). To elucidate the role of p53, a double-Tg mouse line (p53(-/-)/myo(+/+)) was developed by crossing myo-Tg mice with p53-null mice. A significant reduction in cardiac mass with improved cardiac function was observed in p53(-/-)/myo(+/+) mice, suggesting that absence of p53 prevents hypertrophy from turning into HF. Analysis via real-time reverse-transcription PCR revealed changes in transcripts of the p53 pathway in p53(-/-)/myo(+/+) mice. Ingenuity Pathway Analysis indicated that cross-talk among several key nodal molecules (e.g. cyclin-dependent kinase inhibitor 1A, caspase-3, nuclear factor kappa-light-chain enhancer of activated B cells etc.) may play a regulatory role in the transition of CH to HF.
conclusionOur data provide evidence, for the first time, that the coherence of p53 with myo plays an active role during the transition of CH to HF in a model of HF induced by myo overexpression. Transition from CH to HF can be prevented in the absence of p53 in myo-induced hypertrophy. Therefore, deletion/inhibition of p53 could be a therapeutic strategy to prevent CH from transitioning to HF.
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What OpenQuestion holds
Registered trials
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.