ArticlePloS one2016
Paxillin and Focal Adhesion Kinase (FAK) Regulate Cardiac Contractility in the Zebrafish Heart.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 49 citations in OpenAlex.
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- Sirtuin 4 accelerates heart failure development by enhancing reactive oxygen species-mediated profibrotic transcriptional signaling.Journal of molecular and cellular cardiology plus · 2025Article
- Potential of functional flavonoids in targeting vasospasm through modulation of oxidative stress and SPC-induced signaling pathways.Frontiers in pharmacology · 2025Review
- Rbfox1 controls alternative splicing of focal adhesion genes in cardiac muscle cells.Journal of molecular cell biology · 2024Article
- Paxillin participates in the sphingosylphosphorylcholine-induced abnormal contraction of vascular smooth muscle by regulating Rho-kinase activation.Cell communication and signaling : CCS · 2024Article
- Silver Nanoparticles Exposure Impairs Cardiac Development by Suppressing the Focal Adhesion Pathway in Zebrafish.International journal of nanomedicine · 2024Article
- CRISPR/Cas9-mediated nexilin deficiency interferes with cardiac contractile function in zebrafish in vivo.Scientific reports · 2023Article
- CRISPR/Cas9-Mediated Constitutive Loss of VCP (Valosin-Containing Protein) Impairs Proteostasis and Leads to Defective Striated Muscle Structure and Function In Vivo.International journal of molecular sciences · 2022Article
- Proteomic Analysis Suggests Altered Mitochondrial Metabolic Profile Associated With Diabetic Cardiomyopathy.Frontiers in cardiovascular medicine · 2022Article
- Histone deacetylase 1 controls cardiomyocyte proliferation during embryonic heart development and cardiac regeneration in zebrafish.PLoS genetics · 2021Article
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- Modulating hESC-derived cardiomyocyte and endothelial cell function with triple-helical peptides for heart tissue engineering.Biomaterials · 2021Article
- Genetic compensation prevents myopathy and heart failure in an in vivo model of Bag3 deficiency.PLoS genetics · 2020Article
- Proteomic Profiling Reveals Roles of Stress Response, CaAlcoholism, clinical and experimental research · 2020Article
- RNA sequencing-based transcriptome profiling of cardiac tissue implicates novel putative disease mechanisms in FLNC-associated arrhythmogenic cardiomyopathy.International journal of cardiology · 2020Article
- Sequence variants with large effects on cardiac electrophysiology and disease.Nature communications · 2019Article
- Mutations in ILK, encoding integrin-linked kinase, are associated with arrhythmogenic cardiomyopathy.Translational research : the journal of laboratory and clinical medicine · 2019Article
- Unchain My Heart: Integrins at the Basis of iPSC Cardiomyocyte Differentiation.Stem cells international · 2019Review
- MicroRNA-525 enhances chondrosarcoma malignancy by targeting F-spondin 1.Oncology letters · 2019Article
- Semantic Multi-Classifier Systems Identify Predictive Processes in Heart Failure Models across Species.Biomolecules · 2018Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An orchestrated interplay of adaptor and signaling proteins at mechano-sensitive sites is essential to maintain cardiac contractility and when defective leads to heart failure. We recently showed that Integrin-linked Kinase (ILK), ß-Parvin and PINCH form the IPP-complex to grant tuned Protein Kinase B (PKB) signaling in the heart. Loss of one of the IPP-complex components results in destabilization of the whole complex, defective PKB signaling and finally heart failure. Two components of IPP, ILK and ß-Parvin directly bind to Paxillin; however, the impact of this direct interaction on the maintenance of heart function is not known yet. Here, we show that targeted gene inactivation of Paxillin results in progressive decrease of cardiac contractility and heart failure in zebrafish without affecting IPP-complex stability and PKB phosphorylation. However, we found that Paxillin deficiency leads to the destabilization of its known binding partner Focal Adhesion Kinase (FAK) and vice versa resulting in degradation of Vinculin and thereby heart failure. Our findings highlight an essential role of Paxillin and FAK in controlling cardiac contractility via the recruitment of Vinculin to mechano-sensitive sites in cardiomyocytes.
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