Fibrosis in Chronic Inflammatory Diseases

Dear Colleagues,

We are very glad to announce a Special Issue entitled "Fibrosis in Chronic Inflammatory Diseases" that is being prepared for publication in Cells.

Fibrosis, or scarring, is defined by the overgrowth and hardening of tissues due to excess synthesis and deposition of extracellular matrix components. When highly progressive, fibrosis leads to organ dysfunction, accounting for an increasingly large fraction of morbidity and mortality worldwide. In most cases, fibrosis is the end result of chronic inflammation induced by a variety of stimuli such as persistent infections, autoimmune reactions, allergic responses, chemical insults, radiation and tissue injury of different etiologies.

Over the last decade, knowledge regarding the pathophysiology of tissue fibrosis has advanced considerably. A feature common to all fibrotic diseases is the differentiation of extracellular matrix-producing myofibroblasts, which are persistently activated by various profibrotic mechanisms, including paracrine signals derived from inflammatory/immune cells and autocrine factors. Moreover, it is now clear that myofibroblasts can be generated from different cellular sources such as tissue-resident fibroblasts, mesenchymal stromal cells, adipocytes, epithelial and endothelial cells, as well as bone marrow-derived circulating precursors. Significant recent advancements also include the demonstration of common profibrotic molecular pathways across organs, namely transforming growth factor-β, Wnt and hedgehog signaling, among others. Nevertheless, there are still major challenges in the quest to develop effective antifibrotic therapeutic strategies. Indeed, it also appears that the transition from the inflammatory insult to fibrosis and the mechanisms progressing fibrosis may be either common or tissue/disease-specific. Therefore, a deeper understanding of the cellular and molecular mechanisms underlying fibrosis and its relationship with the inflammatory process is necessary to identify new therapeutic targets and increase treatment possibilities.

Outstanding experts interested in this Special Issue are very welcome to submit original manuscripts and reviews dealing with any aspects of the pathogenesis and pathophysiology of fibrosis in chronic inflammatory diseases.

Prof. Dr. Mirko Manetti
Dr. Irene Rosa
Dr. Eloisa Romano
Guest Editors

Dr. Bianca Saveria Fioretto
Guest Editor Assistant

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

• fibrosis
• fibroblasts
• myofibroblasts
• inflammation
• molecular pathways
• pathogenetic mechanisms
• therapeutic targets