Identifying Novel Targets and Mechanisms That Drive Pathogenic Fibrosis and Cancer

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (31 December 2024) | Viewed by 2495

Special Issue Editors


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Guest Editor
Department of Pathology, School of Medicine, Stanford University, Stanford, CA, USA
Interests: innate immunity; fibrosis; genetic reprogramming of fibrotic niches
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Department of Stem Cell Research and Regenerative Medicine, Department of Pathology, School of Medicine, Stanford University, Stanford, CA 94305, USA
Interests: cancer immunology; molecular therapeutics; translational medicine; functional genomics and small molecule inhibitors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Fibrosis and cancer are two major health challenges that affect millions of people worldwide. Fibrosis is a pathological process characterized by excessive deposition of extracellular matrix and inflammation, resulting from a dysregulated response to tissue injury. Cancer is a genetic disease driven by mutations that confer abnormal cell survival, proliferation and dissemination. Although fibrosis and cancer have different origins, they share many common features and mechanisms that influence their development and progression. These include the activation of fibroblasts and immune cells, the production of growth factors and cytokines, the induction of epithelial-to-mesenchymal transition, the generation of oxidative stress and cellular senescence, and the modulation of the Hippo pathway. Moreover, fibrosis and cancer are often intertwined, as fibrotic tissue can provide a pro-tumorigenic microenvironment, and cancer cells can induce fibrosis through paracrine signaling. Therefore, understanding the molecular and cellular interactions between fibrosis and cancer may reveal novel therapeutic targets and strategies for both diseases.

This Special Issue aims to provide a comprehensive overview of the current knowledge and recent advances in the field of fibrosis and cancer immunology. We invite original research articles and reviews that cover various aspects of this topic, such as the molecular mechanisms and signaling pathways involved in fibrosis and cancer, the role of immune cells and inflammation in fibrosis and cancer, the crosstalk between fibrosis and cancer in different organs and tissues, the biomarkers and imaging techniques for fibrosis and cancer diagnosis and prognosis, and the potential therapeutic interventions for fibrosis and cancer. We hope that this Special Issue will stimulate further research and foster collaborations among scientists and clinicians working on fibrosis and cancer immunology

Dr. Gerlinde Wernig
Dr. Cristabelle De Souza
Guest Editors

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Keywords

  • fibrosis
  • cancer
  • extracellular matrix
  • inflammation
  • epithelial-to-mesenchymal transition
  • oxidative stress
  • cellular senescence
  • hippo pathway
  • fibroblast activation

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Published Papers (2 papers)

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16 pages, 4258 KiB  
Article
Lysine Demethylase 1 Has Demethylase-Dependent and Non-Canonical Functions in Myofibroblast Activation in Systemic Sclerosis
by Christopher W. Wasson, Esther Perez Barreiro, Francesco Del Galdo and Natalia A. Riobo-Del Galdo
Cells 2025, 14(6), 433; https://doi.org/10.3390/cells14060433 - 14 Mar 2025
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Abstract
Systemic sclerosis (SSc) is an autoimmune disease of unknown aetiology characterised by vasculopathy with progressive fibrosis of the skin and internal organs. Tissue fibrosis is driven by activated fibroblasts (myofibroblasts) with exacerbated contractile and secretory properties. We previously reported that the long non-coding [...] Read more.
Systemic sclerosis (SSc) is an autoimmune disease of unknown aetiology characterised by vasculopathy with progressive fibrosis of the skin and internal organs. Tissue fibrosis is driven by activated fibroblasts (myofibroblasts) with exacerbated contractile and secretory properties. We previously reported that the long non-coding RNA HOTAIR is a key driver of SSc fibroblast activation. HOTAIR interacts with the chromatin modifiers, the polycomb repressor complex (PRC2) and coREST complex, promoting expression of pro-fibrotic genes. In this study, we show that acute activation of dermal fibroblasts from healthy subjects or SSc patients with transforming growth factor-β and other fibrotic stimuli requires the activity of the lysine-specific demethylase 1 (LSD1) subunit of the co-REST complex. Unexpectedly, LSD1 catalytic activity plays a minor role in fibrotic gene expression in HOTAIR-overexpressing fibroblasts and in maintenance of the stable myofibroblast phenotype of SSc fibroblasts. However, silencing of LSD1 in SSc fibroblasts has a profound effect on pro-fibrotic gene expression, supporting a non-canonical scaffolding function. Our study shows for the first time an essential non-canonical role for LSD1 in pro-fibrotic gene expression in SSc; however, given that this function is insensitive to LSD1 inhibitors, the therapeutic opportunities will depend on future identification of a targetable mediator. Full article
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33 pages, 1974 KiB  
Review
Update of Aging Hallmarks in Idiopathic Pulmonary Fibrosis
by Ana Lilia Torres-Machorro, Ángeles García-Vicente, Marco Espina-Ordoñez, Erika Luis-García, Miguel Negreros, Iliana Herrera, Carina Becerril, Fernanda Toscano, Jose Cisneros and Mariel Maldonado
Cells 2025, 14(3), 222; https://doi.org/10.3390/cells14030222 - 5 Feb 2025
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Abstract
Idiopathic Pulmonary Fibrosis (IPF) is an epithelial-driven interstitial lung disease of unknown etiology characterized by the excessive proliferation of fibroblast populations that synthesize large amounts of extracellular matrix. In this devastating disorder, all aging hallmarks appear prematurely or are altered. This review highlights [...] Read more.
Idiopathic Pulmonary Fibrosis (IPF) is an epithelial-driven interstitial lung disease of unknown etiology characterized by the excessive proliferation of fibroblast populations that synthesize large amounts of extracellular matrix. In this devastating disorder, all aging hallmarks appear prematurely or are altered. This review highlights key findings about IPF characteristics recently recognized as hallmarks of aging, including mechanical alterations, inflammaging, dysbiosis, alternative splicing, and disabled macroautophagy. It also revisits the classic hallmarks of aging, which encompass stem cell exhaustion, cellular senescence, and altered intercellular communication. Enhancing our understanding of the fundamental processes that underlie the altered hallmarks of aging in IPF may facilitate the development of innovative experimental strategies to improve therapeutic outcomes. Full article
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