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      Cyclic nucleotide signalling in kidney fibrosis

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          Abstract

          Kidney fibrosis is an important factor for the progression of kidney diseases, e.g., diabetes mellitus induced kidney failure, glomerulosclerosis and nephritis resulting in chronic kidney disease or end-stage renal disease. Cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) were implicated to suppress several of the above mentioned renal diseases. In this review article, identified effects and mechanisms of cGMP and cAMP regarding renal fibrosis are summarized. These mechanisms include several signalling pathways of nitric oxide/ANP/guanylyl cyclases/cGMP-dependent protein kinase and cAMP/Epac/adenylyl cyclases/cAMP-dependent protein kinase. Furthermore, diverse possible drugs activating these pathways are discussed. From these diverse mechanisms it is expected that new pharmacological treatments will evolve for the therapy or even prevention of kidney failure.

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          Origin and function of myofibroblasts in kidney fibrosis.

          Valerie LeBleu, Gangadhar Taduri, Joyce O'Connell … (2013)
          Myofibroblasts are associated with organ fibrosis, but their precise origin and functional role remain unknown. We used multiple genetically engineered mice to track, fate map and ablate cells to determine the source and function of myofibroblasts in kidney fibrosis. Through this comprehensive analysis, we identified that the total pool of myofibroblasts is split, with 50% arising from local resident fibroblasts through proliferation. The nonproliferating myofibroblasts derive through differentiation from bone marrow (35%), the endothelial-to-mesenchymal transition program (10%) and the epithelial-to-mesenchymal transition program (5%). Specific deletion of Tgfbr2 in α-smooth muscle actin (αSMA)(+) cells revealed the importance of this pathway in the recruitment of myofibroblasts through differentiation. Using genetic mouse models and a fate-mapping strategy, we determined that vascular pericytes probably do not contribute to the emergence of myofibroblasts or fibrosis. Our data suggest that targeting diverse pathways is required to substantially inhibit the composite accumulation of myofibroblasts in kidney fibrosis.
          Article 0 comments Cited 478 times – based on 0 reviews     Review now
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            Mechanisms of TGF-β Signaling from Cell Membrane to the Nucleus

            Yigong Shi, Joan Massagué (2003)
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              Origin of myofibroblasts and cellular events triggering fibrosis.

              Matthias Mack, Motoko Yanagita (2015)
              Renal fibrosis is a major hallmark of chronic kidney disease that is considered to be a common end point of various types of renal disease. To date, the biological meaning of fibrosis during the progression of chronic kidney diseases is unknown and possibly depends on the cell type contributing to extracellular matrix production. During the past decade, the origin of myofibroblasts in the kidney has been intensively investigated. Determining the origins of renal myofibroblasts is important because these might account for the heterogeneous characteristics and behaviors of myofibroblasts. Current data strongly suggest that collagen-producing myofibroblasts in the kidney can be derived from various cellular sources. Resident renal fibroblasts and cells of hematopoietic origin migrating into the kidney seem to be the most important ancestors of myofibroblasts. It is likely that both cell types communicate with each other and also with other cell types in the kidney. In this review, we will discuss the current knowledge on the origin of scar-producing myofibroblasts and cellular events triggering fibrosis.
              Article 0 comments Cited 140 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Ritva Tikkanen: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Int J Mol Sci
                Journal ID (iso-abbrev): Int J Mol Sci
                Journal ID (publisher-id): ijms
                Title: International Journal of Molecular Sciences
                Publisher: MDPI
                ISSN (Electronic): 1422-0067
                Publication date (Electronic): 22 January 2015
                Publication date Collection: February 2015
                Volume: 16
                Issue: 2
                Pages: 2320-2351
                Affiliations
                Pharmacology and Toxicology, University Regensburg, Regensburg 93053, Germany; E-Mails: elisabeth.schinner@ 123456chemie.uni-regensburg.de (E.S.); Veronika.wetzl@ 123456chemie.uni-regensburg.de (V.W.)
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: jens.schlossmann@ 123456chemie.uni-regensburg.de ; Tel.: +49-941-943-4770; Fax: +49-941-943-4772.
                Article
                Publisher ID: ijms-16-02320
                DOI: 10.3390/ijms16022320
                PMC ID: 4346839
                PubMed ID: 25622251
                SO-VID: 51dbf58f-905a-4262-bdb4-2046b21b0e61
                Copyright © © 2015 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 24 October 2014
                Date accepted : 14 January 2015
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular biology
                Keywords: signalling,cyclic nucleotides,cyclic guanosine monophosphate,cyclic adenosine monophosphate,kidney fibrosis
                Data availability:
                ScienceOpen disciplines: Molecular biology
                Keywords: signalling, cyclic nucleotides, cyclic guanosine monophosphate, cyclic adenosine monophosphate, kidney fibrosis

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