Copyright
©The Author(s) 2015. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Exp Med. Nov 20, 2015; 5(4): 200-205
Published online Nov 20, 2015. doi: 10.5493/wjem.v5.i4.200
Published online Nov 20, 2015. doi: 10.5493/wjem.v5.i4.200
Polycystins and mechanotransduction: From physiology to disease
Christina Piperi, Efthimia K Basdra, Department of Biological Chemistry - Cellular and Molecular Biomechanics Unit, Medical School, University of Athens Medical School, 11527 Athens, Greece
Author contributions: Both the authors contributed equally to the conception, writing and critical revision of the manuscript.
Conflict-of-interest statement: Authors declare that there is no conflict of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Efthimia K Basdra, Associate Professor, Department of Biological Chemistry - Cellular and Molecular Biomechanics Unit, Medical School, University of Athens Medical School, 75, M. Asias Street, 11527 Athens, Greece. ebasdra@med.uoa.gr
Telephone: +30-210-7462547 Fax: +30-210-7462703
Received: May 27, 2015
Peer-review started: May 30, 2015
First decision: July 3, 2015
Revised: July 21, 2015
Accepted: September 10, 2015
Article in press: September 16, 2015
Published online: November 20, 2015
Peer-review started: May 30, 2015
First decision: July 3, 2015
Revised: July 21, 2015
Accepted: September 10, 2015
Article in press: September 16, 2015
Published online: November 20, 2015
Core Tip
Core tip: Polycystins are key regulators of mechanosensation in several cell types including kidney, vascular endothelial and smooth muscle cells, osteoblasts and cardiac myocytes. Their expression in primary cilium, plasma membrane and endoplasmic reticulum, along with their ability to interact with diverse ion channels, cell-cell and cell-extracellular matrix junctional proteins renders polycystins as essential regulators of overall cellular mechanoresponse. Abnormal expression or genetic defects of polycystins result in severe structural and mechanosensing faults including cyst formation, deregulated flow sensing, aneurysms, defective bone development and cancer progression, highlighting their crucial role in human physiology.