Novel Targets for Fibrosis Development: Macrophages as a Source of Ligands and Myofibroblast Transition
A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Immunology and Immunotherapy".
Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 21206
Special Issue Editor
2. Centro de Investigación Biomédica en Red Enfermedades Hepáticas y Digestivas (CIBERehd), 46010 Valencia, Spain
Interests: macrophages; fibrosis; TGF; WNT; myofibroblasts; MMT; NOTCH; complications; succinate; autophagy; senescence; chronic inflammation
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Special Issue Information
Dear Colleagues,
Macrophages play an important role in the maintenance of tissue homeostasis; their reply to injury varies immensely depending on the nature and duration of the insult. Macrophages can promote tissue fibrosis, a major driver of progression to end-stage of a lot of diseases (e.g., renal, pulmonary, hepatic or intestinal), via paracrine effects or direct transition to myofibroblast-like cells. Macrophages contribute to fibrosis by dysregulated release of mediators (e.g., TGF-beta, PDGF, VEGF, IGF1, galactin3, WNT ligands) that, acting in a paracrine manner, modulate the function of surrounding cells, including fibroblasts, myofibroblasts and epithelial cells. In addition, recent studies demonstrate that macrophages can directly transform into myofibroblasts within the injured tissue. This process is termed macrophage-to-myofibroblast transition (MMT) and is driven by transforming growth factor-β1 (TGFβ1)-Smad3 signaling. In this regard, therapeutic strategies aimed at controlling macrophage activation, polarization and transition should be emphasized in the prevention of fibrosis.
Prof. Dr. Dolores Ortiz-Masiá
Guest Editor
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Keywords
- Macrophages
- fibrosis
- TGF
- WNT
- myofibroblasts
- MMT
- NOTCH
- complications
- succinate
- autophagy
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