About this Research Topic
Fibrosis is a complex and active process, and is impacted by various cell types, differentiation, and signaling pathways, genes, and cross talks. It is the increased accumulation of fibrous connective tissue in and around tissues with inflammation or damage, which lead to irreversible scar formation and many complications. Understanding the role of inflammatory cells and their mediators in regulation of innate immune cell responses in driving fibrosis deserves further exploration. Ocular fibrosis is associated with various pathologies including glaucoma, diabetes, and age-related macular degeneration, with significant impact on vision. We know very little about the underlying mechanisms involved in ocular fibrosis, the cellular targets, and which are unique or shared with fibrosis in other tissues. Identification of the unique pathways and elucidation of their interactions will allow development of organ specific antifibrotic agents, which are tissue specific and more effective in mitigation of fibrosis.
Despite many efforts in the development of therapies for fibrosis, success has been very limited. Recent advances in single cell omics’ tools are beginning to improve our understanding of the molecular and cellular mechanisms which drive fibrosis and providing new opportunities for more targeted approaches for treatment of fibrosis. The major objective of this series is to advance our understanding of the key molecular and cellular mechanisms, which drive ocular fibrosis. The identity of these pathways may provide novel targets for development of new and effective treatments.
Topics of interest include a) growth factors whose dysregulation contribute to ocular fibrosis; b) the role of various extracellular matrix proteins and their dysregulation in ocular fibrosis; c) the role of inflammatory cells and their mediators in ocular fibrosis; d) the impact of various signaling pathways in ocular fibrosis; e) identification and development of potential targets for treatments of ocular fibrosis; and f) development of strategies to identify new and effective targets for mitigation of ocular fibrosis.
Despite many efforts in the development of therapies for fibrosis, success has been very limited. Recent advances in single cell omics’ tools are beginning to improve our understanding of the molecular and cellular mechanisms which drive fibrosis and providing new opportunities for more targeted approaches for treatment of fibrosis. The major objective of this series is to advance our understanding of the key molecular and cellular mechanisms, which drive ocular fibrosis. The identity of these pathways may provide novel targets for development of new and effective treatments.
Topics of interest include a) growth factors whose dysregulation contribute to ocular fibrosis; b) the role of various extracellular matrix proteins and their dysregulation in ocular fibrosis; c) the role of inflammatory cells and their mediators in ocular fibrosis; d) the impact of various signaling pathways in ocular fibrosis; e) identification and development of potential targets for treatments of ocular fibrosis; and f) development of strategies to identify new and effective targets for mitigation of ocular fibrosis.
Keywords: Ocular fibrosis, molecular, cellular, treatments
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