Biological Functions of Fibroblast Growth Factors (FGFs)
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: closed (1 September 2023) | Viewed by 5733
Special Issue Editors
Interests: FGF; trauma; repair; secretion; signaling; proliferation; differentiation; adipogenesis
Special Issues, Collections and Topics in MDPI journals
Interests: adipogenisis; FGF signaling; metabolic disease; notch signaling; neurogenesis; chemical toxicity
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Fibroblast growth factors (FGFs) comprise a family of ubiquitous and evolutionarily conserved cytokines that are ligands for fibroblast growth factor receptors (FGFRs). FGFRs are transmembrane tyrosine kinases that regulate a wide range of cell fate decisions, including differentiation, proliferation, and death. The expression and availability of FGFs are highly regulated and sensitive to developmental and environmental cues, including those that induce oxidative stress and hypoxia. Inappropriate FGF activity is an underlying contributor to the etiology of developmental disorders and a host of chronic diseases, such as cancer, diabetes, heart diseases, and neuropsychiatric syndromes. This Special Issue explores the role that FGF ligands play in modulating cellular processes during development, in response to environmental stressors, and in the manifestation and progression of disease. Novel FGF research and review articles providing insight into the regulation of FGF activity and signaling in cell culture, animal models, and under-represented biological systems are welcome. The elucidation of the role of FGFs in maintaining and regulating biological functions will increase the future utility of these potent growth factors in the detection, prevention, and/or treatment of a plethora of diseases and disorders.
Dr. Igor A. Prudovsky
Dr. Deena J. Small
Guest Editors
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Keywords
- chronic disease
- cytokine
- development
- FGF
- FGFR
- hypoxia
- oxidative stress
- signal transduction
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