Atrix provoking the loss of lung architecture. Among the excessively produced

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Thus, these enzymes can not only degrade all the components of the extracellular matrix, but they are also able to release, cleave and activate a wide range of growth factors, cytokines, chemokines and cell surface receptors affecting numerous cell functions including adhesion, proliferation, differentiation, recruiting and transmigration, and apoptosis. Therefore, dysregulated expression of MMPs may have profound impact on the biopathological mechanisms implicated in the development of IPF. This review focuses on the current and emerging evidence regarding the role of MMPs on the fibrotic processes in IPF as well as in mouse models of lung fibrosis. Keywords: Lung fibrosis, IPF, Metalloproteinases, Matrisome, MMPBackgroundIdiopathic pulmonary fibrosisIdiopathic pulmonary fibrosis (IPF), the most aggressive fibrotic lung disorder, is a chronic, progressive, irreversible, and usually lethal lung disease of unknown etiology [1, 2]. IPF is an aging-associated disease usually found in people over 50 and its incidence and prevalence increases markedly in the elderly. Although the underlying mechanisms linking aging with IPF are not fully understood, it has been hypothesized that IPF A-836339 chemical information patients may have an accelerated process of lung aging, 4-Hydroxytamoxifen price characterized by increased genomic instability, abnormal shortening of telomeres, epithelial cell senescence, mitochondrial dysfunction, and loss of proteostasis, among others [3, 4]. However, how these mechanisms of aging interrelate is currently largely unknown. In this context, it has been proposed that IPF is the consequence of the convergence* Correspondence: apardos@unam.mx 1 Facultad de Ciencias, Universidad Nacional Aut oma de M ico, M ico, DF, Mexico Full list of author information is available at the end of the articleof three conditions, a genetic architecture that results in an easy loss of the alveolar epithelial integrity, "accelerated" aging, and a distinctive epigenetic "profibrotic" modification [4, 5]. This "mechanistic convergence model" hypothesizes that IPF is driven by the coincidence of multifactorial components which results in a distinct pathogenic cascade leading to the aberrant activation of alveolar epithelial cells [1, 4, 6]. This notion is supported by the presence of increasing numbers of phenotypically varied epithelial cells which are exceptionally title= fnins.2013.00251 active, and synthesize nearly all the mediators that contribute to the formation and activation of the fibroblastic foci and to the progressive and exaggerated accumulation of extracellular matrix. Among these, various MMPs have been found dysregulated and evidence indicates that play a central role not only in the abnormal tissue remodeling but also influencing the epithelial and mesenchymal cell behavior [7] Table title= journal.pone.0077579 1.?2016 Pardo et al. Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomai.Atrix provoking the loss of lung architecture. Among the excessively produced mediators are several matrix metalloproteases (MMPs) which may contribute to modify the lung microenvironment by various mechanisms. Thus, these enzymes can not only degrade all the components of the extracellular matrix, but they are also able to release, cleave and activate a wide range of growth factors, cytokines, chemokines and cell surface receptors affecting numerous cell functions including adhesion, proliferation, differentiation, recruiting and transmigration, and apoptosis. Therefore, dysregulated expression of MMPs may have profound impact on the biopathological mechanisms implicated in the development of IPF.