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Piezo1 acts upstream of TRPV4 to induce pathological changes in endothelial cells due to shear stress

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TLDR
It is demonstrated that Piezo1 activation by fluid shear stress initiates a calcium signal that causes TRPV4 opening, which in turn is responsible for the sustained phase calcium elevation that triggers pathological events in endothelial cells.
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This article is published in Journal of Biological Chemistry.The article was published on 2021-01-01 and is currently open access. It has received 68 citations till now. The article focuses on the topics: Shear stress & Endothelial stem cell.

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Single-cell transcriptomics reveals cell-type-specific diversification in human heart failure

TL;DR: In this article , a comprehensive analysis of the cellular and transcriptomic landscape of human heart failure, identifying cell type-specific transcriptional programs and disease-associated cell states was performed.
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Channelling the Force to Reprogram the Matrix: Mechanosensitive Ion Channels in Cardiac Fibroblasts

TL;DR: A review of mechanosensitive ion channels in cardiac fibroblasts can be found in this article, where the authors discuss evidence of the mechanosensitivity of each channel, and detail the role that each channel plays in cardiac remodelling.
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Piezo1 Channels as Force Sensors in Mechanical Force-Related Chronic Inflammation

TL;DR: This mini-review briefly presents new evidence that Piezo1 responds to different mechanical stresses to trigger inflammation in various tissues and provides new insights for the treatment of chronic inflammatory diseases related to mechanical stress.
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Mechanical Stimulation on Mesenchymal Stem Cells and Surrounding Microenvironments in Bone Regeneration: Regulations and Applications

TL;DR: The mechanotransduction mechanisms of MSCs, the regulation of mechanical stimulation on microenvironments surrounding MSCS by modulating the immune response, angiogenesis and osteogenesis, and the application of mechanical stimulated bone regeneration are reviewed.
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Endothelial shear stress signal transduction and atherogenesis: From mechanisms to therapeutics.

TL;DR: In this article , a review of the recent advances in mechano-transduction and its role in the pathogenesis of atherosclerosis is presented, highlighting the perspective of new anti-atherosclerosis therapies through targeting these mechanoregulated signaling molecules.
References
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Journal ArticleDOI

Flow-mediated endothelial mechanotransduction

TL;DR: The transmission of hemodynamic forces throughout the endothelium and the mechanotransduction mechanisms that lead to biophysical, biochemical, and gene regulatory responses of endothelial cells to hemodynamic shear stresses are reviewed.
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Establishment and characterization of a human acute monocytic leukemia cell line (THP‐1)

TL;DR: Results indicate that THP‐1 is a leukemic cell line with distinct monocytic markers, and the ability to restore T‐lymphocyte response to Con A.
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Piezo1 and Piezo2 Are Essential Components of Distinct Mechanically Activated Cation Channels

TL;DR: Two genes that encode proteins, Piezo1 and Piezo2, are identified, which are required for mechanically stimulated cation conductance in these cells and in cultured dorsal root ganglion neurons, and it is proposed that Piezos are components of MA cation channels.
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Endothelial Cell Dysfunction and the Pathobiology of Atherosclerosis

TL;DR: This review traces the evolution of the concept of endothelial cell dysfunction, focusing on recent insights into the cellular and molecular mechanisms that underlie its pivotal roles in atherosclerotic lesion initiation and progression; explores its relationship to classic, as well as more recently defined, clinical risk factors for atherosclerosis.
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Vanilloid Receptor–Related Osmotically Activated Channel (VR-OAC), a Candidate Vertebrate Osmoreceptor

TL;DR: This work cloned cDNAs encoding the vanilloid receptor-related osmotically activated channel (VR-OAC) from the rat, mouse, human, and chicken, a novel cation-selective channel that is gated by exposure to hypotonicity within the physiological range.
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