ArticleCell death & disease2014
The Hippo pathway is controlled by Angiotensin II signaling and its reactivation induces apoptosis in podocytes.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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60 citing papers in PubMed, 92 citations in OpenAlex.
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- Cardiomyocyte YAP represses myocardial inflammation and fibrosis and restrains MEF2-regulated gene expression.American journal of physiology. Heart and circulatory physiology · 2025Article
- Review
- Modulation of podocyte extracellular matrix remodeling in membranous nephropathy by the NFATc3/LRRC55/BK channel pathway.Journal of cell communication and signaling · 2025Article
- The Hippo Pathway in Kidney Development.Encyclopedia · 2025Article
- Regulation of the Hippo/YAP axis by CXCR7 in the tumorigenesis of gastric cancer.Journal of experimental & clinical cancer research : CR · 2023Article
- The role of the FSGS disease gene product and nuclear pore protein NUP205 in regulating nuclear localization and activity of transcriptional regulators YAP and TAZ.Human molecular genetics · 2023Article
- A YAP/TAZ-ARHGAP29-RhoA Signaling Axis Regulates Podocyte Protrusions and Integrin Adhesions.Cells · 2023Article
- KIBRA upregulation increases susceptibility to podocyte injury and glomerular disease progression.JCI insight · 2023Article
- Aortic Stress Activates an Adaptive Program in Thoracic Aortic Smooth Muscle Cells That Maintains Aortic Strength and Protects Against Aneurysm and Dissection in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Modulation of the hippo-YAP pathway by cyclic stretch in rat type 2 alveolar epithelial cells-a proof-of-concept study.Frontiers in physiology · 2023Article
- Exacerbation of Cisplatin Cellular Toxicity by Regulation of the Human Organic Cation Transporter 2 through Angiotensin II.International journal of molecular sciences · 2022Article
- Effect of Inactivation ofJournal of the Endocrine Society · 2022Article
- O-GlcNAcylation regulation of cellular signaling in cancer.Cellular signalling · 2022Review
- Rho GTPases in kidney physiology and diseases.Small GTPases · 2022Article
- Properties of Transport Mediated by the Human Organic Cation Transporter 2 Studied in a Polarized Three-Dimensional Epithelial Cell Culture Model.International journal of molecular sciences · 2021Article
- Expanding the Spectrum of FAT1 Nephropathies by Novel Mutations That Affect Hippo Signaling.Kidney international reports · 2021Article
- The Hippo pathway: Horizons for innovative treatments of peripheral nerve diseases.Journal of the peripheral nervous system : JPNS · 2021Review
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Authors and funding
11 authors at 2 institutions in 1 country.
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Abstract
The Hippo pathway fulfills a crucial function in controlling the balance between proliferation, differentiation and apoptosis in cells. Recent studies showed that G protein-coupled receptors (GPCRs) serve as upstream regulators of Hippo signaling, that either activate or inactivate the Hippo pathway via the large tumor suppressor kinase (LATS) and its substrate, the co-transcription factor Yes-associated protein (YAP). In this study, we focused on the Angiotensin II type 1 receptor (AT1R), which belongs to the GPCR family and has an essential role in the control of blood pressure and water homeostasis. We found that Angiotensin II (Ang II) inactivates the pathway by decreasing the activity of LATS kinase; therefore, leading to an enhanced nuclear shuttling of unphosphorylated YAP in HEK293T cells. This shuttling of YAP is actin-dependent as disruption of the actin cytoskeleton inhibited dephosphorylation of LATS and YAP. Interestingly, in contrast to HEK293T cells, podocytes, which are a crucial component of the glomerular filtration barrier, display a predominant nuclear YAP localization in vivo and in vitro. Moreover, stimulation with Ang II did not alter Hippo pathway activity in podocytes, which show a deactivated pathway. Reactivation of the LATS kinase activity in podocytes resulted in an increased cytoplasmic YAP localization accompanied by a strong induction of apoptosis. Thus, our work indicates that the control of LATS activation and subsequent YAP localization is important for podocyte homeostasis and survival.
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