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Pathophysiological mechanisms of renal fibrosis: a review of animal models and therapeutic strategies

dc.contributor.authorNogueira, António José M.
dc.contributor.authorPires, Maria João
dc.contributor.authorOliveira, Paula A.
dc.date.accessioned2018-03-26T10:51:15Z
dc.date.available2018-03-26T10:51:15Z
dc.date.issued2017
dc.description.abstractChronic kidney disease (CKD) is a long-term condition in which the kidneys do not work correctly. It has a high prevalence and represents a serious hazard to human health and estimated to affects hundreds of millions of people. Diabetes and hypertension are the two principal causes of CKD. The progression of CKD is characterized by the loss of renal cells and their replacement by extracellular matrix (ECM), independently of the associated disease. Thus, one of the consequences of CKD is glomerulosclerosis and tubulointerstitial fibrosis caused by an imbalance between excessive synthesis and reduced breakdown of the ECM. There are many molecules and cells that are associated with progression of renal fibrosis e.g. angiotensin II (Ang II). Therefore, in order to understand the biopathology of renal fibrosis and for the evaluation of new treatments, the use of animal models is crucial such as: surgical, chemical and physical models, spontaneous models, genetic models and in vitro models. However, there are currently no effective treatments for preventing the progression of renal fibrosis. Therefore it is essential to improve our knowledge of the cellular and molecular mechanisms of the progress of renal fibrosis in order to achieve a reversion/elimination of renal fibrosis.pt_PT
dc.description.sponsorshipThis work was supported in part by a project grant from the Fundação para a Ciência e Tecnologia, Ministério da Educação, Portugal (grant no. SFRH/PROTEC/67576/2010).pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationNogueira, António José M.; Pires, Maria João; Oliveira, Paula Alexandra (2017). Pathophysiological mechanisms of renal fibrosis: a review of animal models and therapeutic strategies. In Vivo. ISSN 0258-851X. 31:1, p. 1-22pt_PT
dc.identifier.doi10.21873/invivo.11019pt_PT
dc.identifier.issn0258-851X
dc.identifier.urihttp://hdl.handle.net/10198/16543
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.relationSFRH/PROTEC/67576/2010pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectAnimalspt_PT
dc.subjectFibrosispt_PT
dc.subjectHumanspt_PT
dc.subjectKidney Diseasespt_PT
dc.subjectDisease Modelspt_PT
dc.subjectAnimalpt_PT
dc.titlePathophysiological mechanisms of renal fibrosis: a review of animal models and therapeutic strategiespt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage22pt_PT
oaire.citation.issue1pt_PT
oaire.citation.startPage1-22pt_PT
oaire.citation.titleIn Vivopt_PT
oaire.citation.volume31pt_PT
person.familyNameNogueira
person.givenNameAntónio José M.
person.identifier.ciencia-id8A11-794E-36BD
person.identifier.orcid0000-0001-8912-7355
person.identifier.scopus-author-id55865568268
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublication648209a2-eec9-4bec-975a-32673e41b95c
relation.isAuthorOfPublication.latestForDiscovery648209a2-eec9-4bec-975a-32673e41b95c

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