Biomechanical Signaling and Fibrosis
A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".
Deadline for manuscript submissions: closed (31 May 2021) | Viewed by 50415
Special Issue Editors
Interests: Rho GTPases; keratinocytes; mouse disease models
Special Issues, Collections and Topics in MDPI journals
Interests: cardiac fibroblasts; fibrosis; biomechanical signalling; mechanotransduction; extracellular matrix
Special Issue Information
Dear Colleagues,
Fibrosis occurs in many different organs as part of various diseases and is involved in about 45% of all deaths. The detrimental effects of fibrosis are often linked to extensive stiffening of the affected tissues, which compromises organ function and affects cellular activity and function. Moreover, the pathological trigger for the development of fibrosis may also involve changes in mechanical properties, e.g., increased blood pressure. Thus, biomechanical signalling is a crucial, but not fully understood, part of fibrotic disease.
Biomechanical signalling can involve the activation of adhesion receptors and mechanosensitive ion channels in the plasma membrane. Cytoskeletal structure and organization affect intracellular signalling molecules and the translocation of transcription factors, thereby regulating fibrotic gene expression programs. Moreover, stiffness of the extracellular environment can affect gene regulation, cytoskeleton-mediated alteration of nuclear shape, chromatin organization and nuclear stiffness.
Whereas many different cell types are affected by fibrosis and tissue stiffening, the fibroblast is central for regulating the development of fibrosis. Fibroblasts are mechanosensitive cells, with great plasticity, that adjust their activity and phenotype according to mechanical signals. The subsequent remodelling of the extracellular matrix will change the mechanical properties of the extracellular environment. Thus, tissue-resident fibroblasts are constantly communicating and striving to obtain a mechanical balance with the surrounding matrix.
Importantly, efficient anti-fibrotic treatment is currently not available, possibly reflecting the lack of understanding of biomechanical signalling in fibrotic disease. This Special Issue will focus on biomechanical signalling mechanisms that regulate and respond to fibrosis in various organs during disease. In addition, in vitro, in vivo and in silico models of fibrotic disease and potential therapeutic strategies are of major interest.
Prof. Dr. Cord Brakebusch
Dr. Kate Møller Herum
Guest Editors
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Keywords
- fibrosis
- mechanotransduction
- disease models
- extracellular matrix
- fibroblasts
- mechanosensing
- ion channels
- Rho GTPase signalling
- computational models
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