ArticleCell death & disease2017
p53-mediated miR-18 repression activates HSF2 for IGF-IIR-dependent myocyte hypertrophy in hypertension-induced heart failure.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled 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.
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
18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 42 citations in OpenAlex.
- Role of miRNA in Cardiovascular Diseases in Children-Systematic Review.International journal of molecular sciences · 2024Pooled it
- Identification of key miRNAs and mRNAs related to coronary artery disease by meta-analysis.BMC cardiovascular disorders · 2021Pooled it
- Diagnostic Value of Let-7a-5p in Essential Hypertension.Journal of clinical hypertension (Greenwich, Conn.) · 2025Article
- Exploring the therapeutic mechanisms of heart failure with Chinese herbal medicine: a focus on miRNA-mediated regulation.Frontiers in pharmacology · 2024Review
- Tripartite motif‑containing 14 may aggravate cardiac hypertrophy via the AKT signalling pathway in neonatal rat cardiomyocytes and transgenic mice.Molecular medicine reports · 2023Article
- Cardiomyocyte Apoptosis Is Associated with Contractile Dysfunction in Stem Cell Model ofInternational journal of molecular sciences · 2023Article
- Cardiomyocyte apoptosis contributes to contractile dysfunction in stem cell model ofbioRxiv : the preprint server for biology · 2023Article
- Autophagic degradation of CCN2 (cellular communication network factor 2) causes cardiotoxicity of sunitinib.Autophagy · 2022Article
- MicroRNAs in cardiovascular diseases.Medical review (2021) · 2022Review
- Upregulation of miR-128 Mediates Heart Injury by Activating Wnt/β-catenin Signaling Pathway in Heart Failure Mice.Organogenesis · 2021Article
- Integrated analysis of the responses of a circRNA-miRNA-mRNA ceRNA network to heat stress in rainbow trout (Oncorhynchus mykiss) liver.BMC genomics · 2021Article
- Insight into the Protective Effect of Salidroside against HOxidative medicine and cellular longevity · 2021Article
- Neurogenic Hypertension Mediated Mitochondrial Abnormality Leads to Cardiomyopathy: Contribution of UPRFrontiers in physiology · 2021Article
- Regulatory RNAs in Heart Failure.Circulation · 2020Review
- Single-cell reconstruction of the adult human heart during heart failure and recovery reveals the cellular landscape underlying cardiac function.Nature cell biology · 2020Article
- Rab9-dependent autophagy is required for the IGF-IIR triggering mitophagy to eliminate damaged mitochondria.Journal of cellular physiology · 2018Article
- Data supporting the angiotensin II activates MEL18 to deSUMOylate HSF2 for hypertension-related heart failure.Data in brief · 2018Article
- Non-coding RNA-linked epigenetic regulation in cardiac hypertrophy.International journal of biological sciences · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypertension-induced cardiac hypertrophy and attenuated cardiac function are the major characteristics of early stage heart failure. Cardiomyocyte death in pathological cardiac conditions is the primary cause of heart failure and mortality. Our previous studies found that heat shock factor 1 (HSF1) protected cardiomyocytes from death by suppressing the IGF-IIR signaling pathway, which is critical for hypertensive angiotensin II-induced cardiomyocyte apoptosis. However, the role of heat shock factor 2 (HSF2) in hypertension-induced cardiac hypertrophy is unknown. We identified HSF2 as a miR-18 target for cardiac hypertrophy. p53 activation in angiotensin II (ANG II)-stimulated NRVMs is responsible for miR-18 downregulation both in vitro and in vivo, which triggers HSF2 expression and the activation of IGF-IIR-induced cardiomyocyte hypertrophy. Finally, we provide genetic evidence that miR-18 is required for cardiomyocyte functions in the heart based on the gene transfer of cardiac-specific miR-18 via adenovirus-associated virus 2 (AAV2). Transgenic overexpression of miR-18 in cardiomyocytes is sufficient to protect against dilated cardiomyopathy during hypertension-induced heart failure. Our results demonstrated that the p53-miR-18-HSF2-IGF-IIR axis was a critical regulatory pathway of cardiomyocyte hypertrophy in vitro and in vivo, suggesting that miR-18 could be a therapeutic target for the control of cardiac functions and the alleviation of cardiomyopathy during hypertension-induced heart failure.
Indexed as
Identifiers
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.