ArticleExperimental and molecular pathology2017
Activation of Yap1/Taz signaling in ischemic heart disease and dilated cardiomyopathy.
Article in Experimental and molecular pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 54 citations in OpenAlex.
- Article
- NUAK1 Inhibition Alleviates Ischemia-Reperfusion Injury via SYNE1-YAP1.Circulation research · 2026Article
- GPCR systems coordinate cellular resilience against aging-associated stress.Frontiers in molecular biosciences · 2026Review
- Microvascular Endothelial Cells License APS Vasculopathy Through YAP1- and CCN2-Mediated Signaling.Circulation · 2025Article
- Network pharmacology combined with experimental analysis to explore the mechanism of the XinShuaiNing formula on heart failure.3 Biotech · 2025Article
- The effects of YAP/TAZ in cardiomyocytes: a scoping review.Molecular biology reports · 2025Article
- TAZ interactome analysis using nanotrap-based affinity purification-mass spectrometry.Journal of cell science · 2025Article
- Cardioprotective mechanism of Qixuan Yijianing formula in Graves' disease mice using miRNA sequencing approach.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- Research progress of ankyrin repeat domain 1 protein: an updated review.Cellular & molecular biology letters · 2024Review
- From gene to mechanics: a comprehensive insight into the mechanobiology of LMNA mutations in cardiomyopathy.Cell communication and signaling : CCS · 2024Review
- Wnt16 Promotes Vascular Smooth Muscle Contractile Phenotype and Function via Taz (Wwtr1) Activation in Male LDLR-/- Mice.Endocrinology · 2023Article
- Article
- A perspective on Notch signalling in progression and arrhythmogenesis in familial hypertrophic and dilated cardiomyopathies.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Cardiac fibroblasts and mechanosensation in heart development, health and disease.Nature reviews. Cardiology · 2023Review
- Network model integrated with multi-omic data predicts MBNL1 signals that drive myofibroblast activation.iScience · 2023Article
- Inhibition of ERK 1/2 pathway downregulates YAP1/TAZ signaling in human cardiomyocytes exposed to hyperglycemic conditions.Biochemical and biophysical research communications · 2023Article
- Yes-Associated Protein and Transcriptional Coactivator with PDZ-Binding Motif in Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- USP15 promotes pulmonary vascular remodeling in pulmonary hypertension in a YAP1/TAZ-dependent manner.Experimental & molecular medicine · 2023Article
- Genetic Ablation ofBiomolecules · 2022Article
- The Hippo Signaling Pathway as a Drug Target in Familial Dilated Cardiomyopathy.International journal of drug discovery and pharmacology · 2022Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
Genetic manipulation of key components of the evolutionally conserved Hippo pathway has shown that the precise control of these signaling molecules is critical to cardiac development and response to stresses. However, how this pathway is involved in the progression of cardiac dysfunction in different heart diseases remains unclear. We investigated the expressional levels and subcellular localization of Yap1, Taz, and Tead1 and determined Hippo target gene expression in failing human hearts with ischemic heart disease (IHD) and idiopathic dilated cardiomyopathy (IDC) and mouse desmin-related cardiomyopathy (DES). Our results demonstrated that Yap1, Taz, and Tead1 were significantly increased in failing human and DES hearts compared with the non-failing controls (NFH) or wild type (WT) mouse hearts at both mRNA and protein levels. Interestingly, adult human and mouse hearts had more Taz than Yap1 by mRNA and protein expression and their increases in diseased hearts were proportional and did not change Yap1/Taz ratio. Yap1, Taz, and Tead1 were accumulated in the nuclear fraction and cardiomyocyte nuclei of diseased hearts. The ratio of Yap1 phosphorylated at serine 127 (human) or serine 112 (mouse) to the total Yap1 (pYap1/Yap1) was significantly lower in the nuclear fraction of diseased hearts than that in normal controls. More importantly, Hippo downstream targets Ankrd1, Ctgf, and Cyr61 were transcriptionally elevated in the diseased hearts. These results suggest that Yap1/Taz signaling is activated in human and mouse dysfunctional hearts. Further investigation with relevant animal models will determine whether this pathway is a potential target for preventing and reversing abnormal remodeling during the progression of different cardiac disorders.
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Registered trials
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