Research Topic

Molecular Mechanisms and New Therapeutic Targets in Epithelial to Mesenchymal Transition (EMT) and Fibrosis

About this Research Topic

The induction of inflammatory EMT/fibrosis requires a complex cellular reprogramming process involving epithelial, stromal, immune cells, and has important implications on cell survival, plasticity and migratory/invasive abilities.
A wide array of extracellular stimuli, including soluble mediators, cell-to-cell interactions, binding to Extracellular matrix (ECM), drive changes in resident cells towards a mesenchymal-like/pro-fibrotic phenotype. Moreover, seminal studies have demonstrated that, in addition to biochemical extracellular signals, biomechanical cues may play a key role in the induction of cellular changes associated with these processes.
Besides the classical pathways induced by TGF-β the main profibrotic mediator (i.e. the SMADs and MAPK signalling pathways), the roles of new intracellular mechanisms in the modulation of EMT/fibrosis are being elucidated. In particular, the discovery of microRNA and, more recently, of long nonconding RNA (lincRNA), added new layers of regulation. At the same time, processes such as histone acetylation and DNA/histone methylation impact on the persistence of a new mesenchymal-like state or on the reversion to an epithelial-like phenotype (MET). However, despite mounting efforts in the field, new mechanisms remain to be elucidated, and cell-type specificities have yet to be fully characterized.
In this Research Topic, we wish to provide a timely overview of disease- and organ-specific triggers associated with the induction and perpetuation of EMT induction and fibrogenesis. Moreover, we would like to provide insight on new strategies aimed to counteract organ fibrosis, thereby providing new clues for potential anti-fibrotic targets.
A deeper knowledge of these mechanisms is relevant from both the basic and translational points of view, as it clarifies basic physio-pathological processes (e.g. wound healing, organ fibrosis, cell migration/invasion in tumoral and non-tumoral conditions), and can be harnessed to develop regenerative medicine strategies and complex biomaterials to control EMT and fibrotic responses in specific and localized manners.


Keywords: EMT, Fibrosis, epigenetics, therapeutic targets, biomaterials


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

The induction of inflammatory EMT/fibrosis requires a complex cellular reprogramming process involving epithelial, stromal, immune cells, and has important implications on cell survival, plasticity and migratory/invasive abilities.
A wide array of extracellular stimuli, including soluble mediators, cell-to-cell interactions, binding to Extracellular matrix (ECM), drive changes in resident cells towards a mesenchymal-like/pro-fibrotic phenotype. Moreover, seminal studies have demonstrated that, in addition to biochemical extracellular signals, biomechanical cues may play a key role in the induction of cellular changes associated with these processes.
Besides the classical pathways induced by TGF-β the main profibrotic mediator (i.e. the SMADs and MAPK signalling pathways), the roles of new intracellular mechanisms in the modulation of EMT/fibrosis are being elucidated. In particular, the discovery of microRNA and, more recently, of long nonconding RNA (lincRNA), added new layers of regulation. At the same time, processes such as histone acetylation and DNA/histone methylation impact on the persistence of a new mesenchymal-like state or on the reversion to an epithelial-like phenotype (MET). However, despite mounting efforts in the field, new mechanisms remain to be elucidated, and cell-type specificities have yet to be fully characterized.
In this Research Topic, we wish to provide a timely overview of disease- and organ-specific triggers associated with the induction and perpetuation of EMT induction and fibrogenesis. Moreover, we would like to provide insight on new strategies aimed to counteract organ fibrosis, thereby providing new clues for potential anti-fibrotic targets.
A deeper knowledge of these mechanisms is relevant from both the basic and translational points of view, as it clarifies basic physio-pathological processes (e.g. wound healing, organ fibrosis, cell migration/invasion in tumoral and non-tumoral conditions), and can be harnessed to develop regenerative medicine strategies and complex biomaterials to control EMT and fibrotic responses in specific and localized manners.


Keywords: EMT, Fibrosis, epigenetics, therapeutic targets, biomaterials


Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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Submission Deadlines

30 January 2018 Abstract
30 July 2018 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

30 January 2018 Abstract
30 July 2018 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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