Special Issue "Links between Fibrogenesis and Cancer: Mechanistic and Therapeutic Challenges"
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: closed (30 June 2019).
Fibrosis is the end-stage of many chronic inflammatory diseases. It is associated with progressive scarring of an organ with reduction or loss of function. Scarring of parenchymal organs is characterized by abnormally-enhanced tissue deposition of extracellular matrix components, including several types of collagens, fibronectin and matricellular proteins, such as tenascin and periostin. The process is generally reversible at early stages, but it becomes irreversible with advanced disease. However, the point of no return is unknown. We address this question in this Special Issue with original research or reviews dealing with factors or biomarkers of fibrosis irreversibility.
Tissue fibrosis may be the consequence of different pathological states, including chronic inflammatory or infectious diseases, autoimmune disorders, graft rejection and malignancy; but in some diseases, such as idiopathic pulmonary fibrosis, the cause is unknown and the fibrotic process progresses despite the absence of conspicuous inflammation. Irrespective of the underlying pathological condition, tissue with ongoing fibrogenesis has a high content of matrix proteins and myofibroblasts activated by various pro-fibrotic factors among which transforming growth factor-β1 plays a critical role. However, the stimulus that perpetuates the secretion or increases the level and activation of transforming growth factor-β1 during fibrogenesis is unclear. Therefore, studies on genetic factors or environmental agents (e.g., microbiota) playing a role in the excessive and persistent growth factor activity during fibrotic processes will be part of this issue.
Disruption of organ parenchymal cells and of the normal organ structural scaffold during organ fibrogenesis causes loss of cell polarity that may promote uncontrolled cell proliferation leading eventually to cancer onset and progression. Tumors have been identified in fibrotic tissues decades ago and now it is well-recognized that fibrotic lesions enhance the risk of cancer in several organs such liver, lung and breast. The mechanism linking fibrosis and cancer is unknown. This Special Issue will address cellular and molecular abnormalities including aberrant expression of microRNAs, genetic and epigenetic alterations, evasion or delayed apoptosis, unregulated intracellular signal pathways, and dysregulation or defective intercellular communications that may provide insights to explain the pathological link between fibrogenesis and carcinogenesis.
The pathogenic role of myofibroblasts is common in both fibrosis and cancer. Myofibroblasts are the main source of matrix proteins and their enhanced activity is an important prognostic indicator in patients with either organ fibrosis or malignancy. Comparative studies evaluating the phenotypic, behavioral, biochemical and molecular alterations in myofibroblasts may help developing drugs equally effective for both disease conditions. For example, the multi-kinase inhibitor nintedanib was initially developed for use as an anti-cancer drug but was subsequently approved for treating lung fibrosis. This is because targeted receptors were also found to be abnormally activated in lung fibrosis. Research covering these topics will also be part of this Special Issue.
Topics for this Special Issue include, but are not limited to:
- Matricellular proteins
- Regulatory mechanism of secretion and activation of transforming growth factor-beta1 and other pro-fibrotic factors.
- Myofibroblasts from fibrotic tissue and cancerous tissues
- Epithelial or endothelial mesenchymal transition during fibrinogenesis and carcinogenesis
- Microbiome in fibrosis and cancer
- New therapeutic agents for organ fibrosis and cancer
- Interaction of myofibroblasts with extracellular matrix proteins
- Intracellular signal pathways controlling the expression of extracellular matrix proteins.
- Animal models of fibrosis and/or cancer
- Diagnostic approaches for lung fibrotic diseases and cancer.
Prof. Dr. Esteban C. Gabazza
Manuscript Submission Information
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- Fibrosis-associated cancer
- Endothelial mesenchymal transition
- Profibrotic cytokines
- Cancer resistance to therapy
- Experimental animal models