ArticleThe Journal of biological chemistry2017
Focal Adhesion Kinase-mediated Phosphorylation of Beclin1 Protein Suppresses Cardiomyocyte Autophagy and Initiates Hypertrophic Growth.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
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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.
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Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- Shen-yuan-dan capsule inhibits METTL3-mediated m6A methylation to restore autophagy homeostasis and attenuate post-myocardial infarction heart failure.Frontiers in pharmacology · 2026Article
- Autophagy fine-tuning by angiotensin-(1-9) in cultured rat cardiomyocytes.Frontiers in cardiovascular medicine · 2025Article
- THSD1 Suppresses Autophagy-Mediated Focal Adhesion Turnover by Modulating the FAK-Beclin 1 Pathway.International journal of molecular sciences · 2024Article
- Strategies adopted by Salmonella to survive in host: a review.Archives of microbiology · 2023Review
- Autophagy, molecular chaperones, and unfolded protein response as promoters of tumor recurrence.Cancer metastasis reviews · 2023Review
- Genome-Wide Analysis of Left Ventricular Maximum Wall Thickness in the UK Biobank Cohort Reveals a Shared Genetic Background With Hypertrophic Cardiomyopathy.Circulation. Genomic and precision medicine · 2023Article
- Article
- Biphasic Functions of Sodium Fluoride (NaF) in Soft and in Hard Periodontal Tissues.International journal of molecular sciences · 2022Review
- Review
- Emerging therapeutic targets for cardiac hypertrophy.Expert opinion on therapeutic targets · 2022Review
- Strain-induced mechanoresponse depends on cell contractility and BAG3-mediated autophagy.Molecular biology of the cell · 2021Article
- Cell type-specific roles of PAR1 in Coxsackievirus B3 infection.Scientific reports · 2021Article
- Review
- Comprehensive analysis of autophagy-related genes and patterns of immune cell infiltration in valvular atrial fibrillation.BMC cardiovascular disorders · 2021Article
- The Road of Solid Tumor Survival: From Drug-Induced Endoplasmic Reticulum Stress to Drug Resistance.Frontiers in molecular biosciences · 2021Review
- Regulation of Beclin 1-Mediated Autophagy by Oncogenic Tyrosine Kinases.International journal of molecular sciences · 2020Review
- FAK Signaling in Rhabdomyosarcoma.International journal of molecular sciences · 2020Review
- ATM-CHK2-Beclin 1 axis promotes autophagy to maintain ROS homeostasis under oxidative stress.The EMBO journal · 2020Article
- Doxorubicin induces cardiomyocyte apoptosis and atrophy through cyclin-dependent kinase 2-mediated activation of forkhead box O1.The Journal of biological chemistry · 2020Article
- Deregulation of autophagy is involved in nephrotoxicity of arsenite and fluoride exposure during gestation to puberty in rat offspring.Archives of toxicology · 2020Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Autophagy is an evolutionarily conserved intracellular degradation/recycling system that is essential for cellular homeostasis but is dysregulated in a number of diseases, including myocardial hypertrophy. Although it is clear that limiting or accelerating autophagic flux can result in pathological cardiac remodeling, the physiological signaling pathways that fine-tune cardiac autophagy are poorly understood. Herein, we demonstrated that stimulation of cardiomyocytes with phenylephrine (PE), a well known hypertrophic agonist, suppresses autophagy and that activation of focal adhesion kinase (FAK) is necessary for PE-stimulated autophagy suppression and subsequent initiation of hypertrophic growth. Mechanistically, we showed that FAK phosphorylates Beclin1, a core autophagy protein, on Tyr-233 and that this post-translational modification limits Beclin1 association with Atg14L and reduces Beclin1-dependent autophagosome formation. Remarkably, although ectopic expression of wild-type Beclin1 promoted cardiomyocyte atrophy, expression of a Y233E phosphomimetic variant of Beclin1 failed to affect cardiomyocyte size. Moreover, genetic depletion of Beclin1 attenuated PE-mediated/FAK-dependent initiation of myocyte hypertrophy
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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.