About this Research Topic
Fibrosis, a hallmark of many chronic degenerative disorders, is associated with reduced organ function and eventual organ failure. Fibrotic disease is on the increase; for example, idiopathic pulmonary fibrosis (IPF), the most common type of idiopathic interstitial pneumonia, occurs with similar frequency to that of stomach, brain and testicular cancer. The current anti-fibrotic therapeutics (such as pirfenidone and nintedanib) are of limited efficacy and, at present, organ transplantation, when possible, represents the only option, even if all the related concerns must be considered. Therefore, the identification of alternative and effective therapies aiming to prevent and even more, to revert excessive tissue scarring is a current scientific challenge and an urgent medical need with high impact on health care system.
To accomplish this task, it appears necessary to systematically underpin the pathogenesis of pulmonary fibrosis. To date, injury to and/or dysfunction of alveolar epithelium is strongly implicated in the initiation of IPF, but what factors determine why fibrosis progresses rather than normal tissue repair occurs, remain poorly understood. Although generations of myofibroblasts and their persistence in the activated functional state are considered as key disease drivers; other cells, such as epithelial cells, endothelial cells, adipocyte/adipose-derive stem cells, pericytes, monocytes/macrophages have been suggested as potential modulators of tissue scarring.
In this Research Topic, contributions are encouraged to further and more deeply investigate the aetiology, genetics and genomics, cell types and the molecular mechanisms involved in the onset and progression of pulmonary fibrosis.
This Research Topic will highlight the relevance of this area and the current trends. It will provide new insights into cellular players and molecular signaling pathways which drive fibrosis and can potentially accelerate the identification of biomarkers and development of effective treatment.
Topics covered may include, but are not limited to, the following:
• Aetiology
• Genetics and Genomics
• Mechanisms
• Biomarkers
• Pharmacologic treatment
• Models of disease
To accomplish this task, it appears necessary to systematically underpin the pathogenesis of pulmonary fibrosis. To date, injury to and/or dysfunction of alveolar epithelium is strongly implicated in the initiation of IPF, but what factors determine why fibrosis progresses rather than normal tissue repair occurs, remain poorly understood. Although generations of myofibroblasts and their persistence in the activated functional state are considered as key disease drivers; other cells, such as epithelial cells, endothelial cells, adipocyte/adipose-derive stem cells, pericytes, monocytes/macrophages have been suggested as potential modulators of tissue scarring.
In this Research Topic, contributions are encouraged to further and more deeply investigate the aetiology, genetics and genomics, cell types and the molecular mechanisms involved in the onset and progression of pulmonary fibrosis.
This Research Topic will highlight the relevance of this area and the current trends. It will provide new insights into cellular players and molecular signaling pathways which drive fibrosis and can potentially accelerate the identification of biomarkers and development of effective treatment.
Topics covered may include, but are not limited to, the following:
• Aetiology
• Genetics and Genomics
• Mechanisms
• Biomarkers
• Pharmacologic treatment
• Models of disease
Keywords: Aetiology, Genetics and Genomics, Mechanisms, Biomarkers, Pharmacologic treatment, Models of disease
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.
