Organ and Tissue Fibrosis: Molecular Signals and Cellular Mechanisms—Second Edition

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Tissues and Organs".

Deadline for manuscript submissions: 15 December 2025 | Viewed by 589

Special Issue Editor

School of Life and Health Sciences, Aston University, Birmingham, UK
Interests: fibrotic diseases; cancer and pathological angiogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue of Cells is dedicated to the molecular signals and cellular mechanisms of organ and tissue fibrosis. Fibrosis is characterised as the formation and remodelling of scar tissue and is an end result of many conditions, such as injury and inflammation. Fibrosis leads to the loss of tissue and organ functions, while fibrotic disorders contribute to around 40% of all causes of mortality. Even though fibrosis occurs in the extracellular matrix, understanding the role of cells and molecular signals in organ fibrosis is important to enhance our knowledge of this pathological process and eventually develop effective treatments. This Special Issue will focus on various cellular and molecular mechanisms during fibrosis in various organs, such as inflammatory cytokine-induced cell transition into myofibroblasts. This Special Issue will contain both original research articles and reviews. Studies performed using in vitro, ex vivo and in vivo models are welcome.

Dr. Zhuo Wang
Guest Editor

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Keywords

  • fibrosis
  • scarring
  • cytokine
  • myofibroblasts
  • extracellular matrix
  • growth factors
  • mesenchymal transition

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Published Papers (1 paper)

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Review

24 pages, 2082 KB  
Review
Understanding the Mechanisms Driving Fibrosis Following Cochlear Implantation—Lessons from Other Tissues
by Cecilia M. Prêle, Kady J. Braack, Marcus Atlas, Jafri Kuthubutheen, Tylah Miles, Wilhelmina H. A. M. Mulders and Steven E. Mutsaers
Cells 2025, 14(23), 1924; https://doi.org/10.3390/cells14231924 - 3 Dec 2025
Viewed by 430
Abstract
Cochlear implants are highly successful in restoring speech perception but variability in outcomes exists. Post-surgical fibrosis and neo-ossification are thought to play a significant role, being linked to increased impedance and loss of residual hearing and posing challenges for re-implantation. Hence, there is [...] Read more.
Cochlear implants are highly successful in restoring speech perception but variability in outcomes exists. Post-surgical fibrosis and neo-ossification are thought to play a significant role, being linked to increased impedance and loss of residual hearing and posing challenges for re-implantation. Hence, there is growing interest in pharmacological interventions to limit intracochlear fibrosis and neo-ossification. While current approaches focus on steroids, studies in other organs have identified many candidate drugs. However, selection is hindered by a limited understanding of the molecular and cellular mechanisms driving fibrosis after implantation. This review introduces potential drug candidates for cochlear implant-induced fibrosis, with many targeting core fibrotic pathways such as TGF-β/SMAD, PDGF, and Wnt/β-catenin or inhibiting pro-inflammatory signalling. By drawing on lessons from other tissues, this review identifies mechanisms and therapeutic approaches adaptable to the cochlea. Understanding fibrosis across organs will guide strategies to prevent or reverse cochlear fibrosis. Their translation requires careful evaluation of local delivery, minimal ototoxicity, and effects on the electrode–tissue interface. Full article
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