Cellular Mechanisms and Signaling Pathways in Normal Tissue Repair and Fibrosis
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: 29 June 2025 | Viewed by 122
Special Issue Editors
Interests: cell biology and signal transduction of normal tissue repair and fibrotic remodeling in the lung; adult stem cells that participate in lung repair; apoptosis; cytoskeletal rearrangement; cellular senescence and inflammation; reactive oxygen species in signal transduction and antioxidant cellular defenses
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Fibrotic disorders have been described for all organs, including the heart, liver, kidney, lung, spleen, pancreas, thymus, lymph nodes, bone marrow, brain, skin, gastrointestinal tract, eyes, etc. For many of these organs, the events initiating fibrosis are not well defined, although in some cases, the process appears to involve inflammation and/or tissue injury followed by failed repair, ultimately resulting in fibrotic remodeling. For many of these diseases, fibrosis is progressive, and reversal of fibrosis to form functional tissue has not been described. Recent research describes novel molecular and biochemical pathways involved in fibrotic remodeling and the development of animal models that recapitulate the human diseases.
For this Special Issue, we would like to invite papers that investigate molecular and cellular mechanisms for the initiation and progression of fibrosis and the discovery of antifibrotics. Some potential topics include:
- The relationship between inflammation/inflammatory responses and fibrotic remodeling.
- The accelerated senescence or loss of adult stem cells in a tissue and the activation of fibrotic remodeling as a response to loss of normal tissue turnover.
- The activation of novel signaling pathways that may initiate or perpetuate fibrosis and inhibit normal tissue repair.
- Novel animal models for the testing and development of antifibrotic agents.
- Agents that delay, suppress, or reverse fibrotic remodeling.
This Special Issue is calling for both original articles and reviews providing to the readers of IJMS comprehensive reviews of fibrosis pathways in any one organ system or a comparison of fibrotic pathways in multiple organs, highlighting similarities and differences.
Prof. Dr. Regina M. Day
Dr. Jeffrey R. Koenitzer
Guest Editors
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Keywords
- fibrosis
- inflammation
- senescence
- myofibroblasts
- Wnt/hedgehog
- extracellular matrix
- hedgehog
- angiotensin II/transforming growth factor-beta
- ephrins
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