Inflammation and fibrosis are pivotal processes associated with a myriad of diseases. When prompted by trauma, aging, or stress stimuli, the immune system becomes activated, leading to a cascade of inflammatory responses initiated by macrophages, T cells, and other immune players. Typically, inflammation sets the stage for fibrotic progression, characterized by the differentiation of myofibroblasts and significant extracellular matrix deposition. The extracellular matrix, rich in collagen, not only occupies substantial tissue space and diminishes organ functionality but also perpetuates chronic inflammation. Specifically, the intercellular interplay, such macrophage-fibroblast cross-talk, macrophage stromal cell cross-talk et al., has a key role in the progress of inflammation-fibrosis interaction. On the other hand, despite the extensive presence of these conditions in various disorders, effective therapeutic options remain limited.
The advancements in multi-omic tools and experimental technologies now provide opportunities to uncover the intricate relationships between inflammation and fibrosis, highlighting roles of cellular components, intercellular communication, and cell-matrix interactions. These insights are paving the way for the discovery of novel therapeutic agents to disrupt this vicious cycle.
This Research Topic aims to present new findings regarding the causal interactions between inflammation and fibrosis, explore cellular roles during transitions between the two, and identify novel molecules/therapies that could modulate these processes using integrative approaches. We welcome contributions from both clinical and basic research domains, along with comprehensive reviews.
To gain a deeper understanding of the intricacies involved in inflammation-fibrosis interactions, this Research Topic invites a wide array of studies focusing on the molecular regulation, functional validation, causal link, and translational investigations of these processes. Recommended topics include, but are not limited to:
• The mechanisms facilitating the transition from inflammation to fibrosis and vice versa. • The origin and role of myofibroblasts within inflammatory environments • Experimental-based development of anti-fibrotic agents • Epigenetic influences on inflammation and fibrosis • Biomarkers for predicting fibrosis after inflammatory stimulation • Designation and verification of biomaterials targeting inflammation or fibrosis • Multi-omic studies with single cell technique, spatial technique et al. • Clinical analysis unveiling the shift or transition from inflammation to fibrosis
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This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:
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Methods
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Article types
This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:
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