Molecular Mechanisms in Organ Fibrosis

Dear colleagues,

Fibrosis is a dynamic process which is mainly characterized by an excessive accumulation of extracellular matrix. Fibrosis generally occurs as an uncontrolled wound-healing response to multiple and chronic injuries. It induces the alteration of organ architecture and leads to loss of organ function. Fibrosis is a pathology that affects several organs such as the kidney, lungs, liver, skin, peritoneum, and heart. In addition, even if the main source of the extracellular matrix is activated myofibroblasts, a great many cell types modulate the phenomenon (epithelial and mesothelial cells, endothelial cells, pericytes, vascular smooth muscle cells, inflammatory cells, and mesenchymal stem cells). Commonly, the fibrotic process is initiated by parenchymal damage followed by an unsolved inflammation, and thus, some molecular mechanisms at the origin of fibrosis are shared by different organs. In this scenario, additional tissue-specific mechanisms are responsible for fibrosis. Keeping in mind that in certain situations, fibrosis could be a reversible process, a deeper knowledge of its foundation is highly necessary in order to develop new therapeutic strategies.

The aim of this Special Issue of Cells is to report new findings that advance knowledge of the molecular mechanisms of organ fibrosis. We welcome submissions of research papers and reviews that focus on aspects of known mechanisms/pathways such as epithelial–mesenchymal transition, TGF-beta signaling, myofibroblast activation, proliferation, and senescence, but also manuscripts exploring new aspects.

Prof. Maurizio Onisto
Dr. Valentina Masola
Guest Editors

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