Molecular Mechanism in Epithelial-Mesenchymal Transition (EMT) and Fibrosis: 2nd Edition
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".
Deadline for manuscript submissions: 20 December 2024 | Viewed by 3240
Special Issue Editors
Interests: autoimmunity; Sjogren’s syndrome; inflammation; salivary gland dysfunction; epithelial–mesenchymal transition; fibrosis
Special Issues, Collections and Topics in MDPI journals
Interests: pathophysiology and molecular immunology applied to immunological research lines; molecular processes underlying the interaction between receptors of the immune response, inflammation and characterization of new anti-inflammatory molecules; novel therapies for Sjögren’s syndrome autoimmune disease; evaluation of the molecular mechanisms linking chronic inflammation to fibrosis in Sjögren’s syndrome and others autoimmune diseases
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
The process known as epithelial–mesenchymal transition (EMT), essential for accurate development during embryogenesis, is involved in many pathological processes, such as degenerative fibrosis and cancer. EMT is a biological process that allows epithelial cells to assume a mesenchymal phenotype with enhanced migratory capacity, invasiveness, elevated resistance to apoptosis, stem-like features, and the increased production of ECM components.
During EMT, distinct molecular processes are activated: the loss of junctions and apical–basal polarity by epithelial cells, the activation of transcription factors, the downregulation of epithelial cell-surface proteins and upregulation of mesenchymal markers, and the reorganization and expression of cytoskeletal proteins.
EMT is linked to wound healing, tissue regeneration, and organ fibrosis. During the course of fibrosis, EMT can lead to organ failure following the persistent release of a variety of inflammatory signals.
EMT is now considered to be a converging point among inflammation, fibrotic diseases, cancer, and pathologies characterized by chronic inflammation, such as autoimmune diseases. However, despite intense investigation in recent years, relatively little is known about the mechanisms of fibrosis pathogenesis and how all of these events are integrated and participate in the same process, and how the mesenchymal state is maintained. Deep knowledge of these aspects will help to exploit the plasticity of this process to reverse the metastatic phenotype of many cancers and design potential therapeutic approaches.
Papers related to any aspect of EMT and fibrosis will be considered for publication within this Special Issue.
Dr. Sabrina Lisi
Dr. Margherita Sisto
Guest Editors
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Keywords
- inflammation
- cancer
- EMT
- autoimmunity
- fibrosis
- salivary glands
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