Mangolini A, de Stephanis L, Aguiari G. Role of calcium in polycystic kidney disease: From signaling to pathology. World J Nephrol 2016; 5(1): 76-83 [PMID: 26788466 DOI: 10.5527/wjn.v5.i1.76]
Corresponding Author of This Article
Gianluca Aguiari, PhD, Department of Biomedical and Surgical Specialty Sciences, Section of Biochemistry, Molecular Biology and Medical Genetics, University of Ferrara, via Fossato di Mortara 74, 44121 Ferrara, Italy. dsn@unife.it Telephone: +39-532-974460
Research Domain of This Article
Biochemistry & Molecular Biology
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
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/
World J Nephrol. Jan 6, 2016; 5(1): 76-83 Published online Jan 6, 2016. doi: 10.5527/wjn.v5.i1.76
Role of calcium in polycystic kidney disease: From signaling to pathology
Alessandra Mangolini, Lucia de Stephanis, Gianluca Aguiari
Alessandra Mangolini, Lucia de Stephanis, Gianluca Aguiari, Department of Biomedical and Surgical Specialty Sciences, Section of Biochemistry, Molecular Biology and Medical Genetics, University of Ferrara, 44121 Ferrara, Italy
Alessandra Mangolini, Department of Morphology, Surgery and Experimental Medicine, Section of Pathology, Oncology and Experimental Biology, University of Ferrara, 44121 Ferrara, Italy
Author contributions: Mangolini A and de Stephanis L performed the experiments; Aguiari G generated the figures and wrote the manuscript.
Supported by University of Ferrara local funds: FAR 2012, 2013, 2014 and Regione Emilia Romagna grant (Ricerca Regione-Università) 2007-2009.
Conflict-of-interest statement: The authors declare that they have no commercial, personal, political, intellectual or religious conflict of interests regarding the data or scientific reports included in the present article. There is no conflict of interest associated with the senior author or other coauthors contributed their efforts in this paper.
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: Gianluca Aguiari, PhD, Department of Biomedical and Surgical Specialty Sciences, Section of Biochemistry, Molecular Biology and Medical Genetics, University of Ferrara, via Fossato di Mortara 74, 44121 Ferrara, Italy. dsn@unife.it Telephone: +39-532-974460
Received: September 9, 2015 Peer-review started: September 10, 2015 First decision: October 8, 2015 Revised: November 21, 2015 Accepted: December 8, 2015 Article in press: December 11, 2015 Published online: January 6, 2016
Core Tip
Core tip: In the present article, we discuss: (1) the regulation of calcium signaling in the primary cilia of autosomal dominant polycystic kidney disease (ADPKD) cells and the downstream processes that lead to cystogenesis; (2) how calcium impairment promotes cell proliferation by activating different signaling pathways; (3) the activity of non-capacitative calcium entry channels, which in PKD1-silenced cells stimulates cell growth by Ca2+ oscillations and nuclear factor of activated T-cells activation, highlighting new findings showing the role of polycystin-2 in calcium oscillations; (4) the impairment of intracellular calcium signaling associated with apoptosis; and (5) the use of calcium channel blockers and calcium modulators in the treatment of ADPKD.
