About this Research Topic
Transcription factor (TF) manages the production of diverse pro-inflammatory and destructive molecules, so regulation of TF can affect the formation of inflammation or fibrosis. Macrophages, including a heterogeneous group of phenotypically and genetically distinct immue cells, also control initiations and progression of inflammation and fibrosis. Regulation of macrophages are associated to a complex regulatory network of TF families, such as nuclear factor kappa B (NF-κB) and activator protein 1 (AP-1), Fos-related antigen 1 (Fra-1), cyclic AMP response element (CRE)-binding protein (CREB), and CCAAT enhancer-binding protein (CEBP). In this Research Topic, we will focus on the regulation mechanism on TF in inflammation and/or fibrosis.
With the Research Topic, we will explore the currently practical unmet needs in inflammation and fibrosis research and clinical practice, as well as fields where urgent progress will be needed in the near future. We welcome submissions covering, but not limited to the following areas:
The mechanisms by which macrophages acquire pro-inflammatory or an-inflammatory lineages and the signaling involved in their transition to these lineages during injury remains a topic of debate. When will TFs be activated to inhibit inflammation or fibrosis? Does overactivation cause inflammation or fibrosis? When does TF activation lead to full restoration and when just to inflammation or fibrosis? Does inhibition of inflammation prevent fibrosis?
Also, DNA methylation can alter TF-DNA binding and function. The association of TFs with each other and with co-activating/repressing proteins are determined by the modular structure of the TFs and the presence of distinct interacting domains. What are the new methylation modifications that have been discovered? What are the new TF binding sites?
Finally, post-translational modifications of TFs by phosphorylation, acetylation, ubiquitination, and nitration can have profound effects on either the DNA-binding capacity or the transcriptional activity of TFs. What are the new post-translational modifications that have been found?
With the Research Topic, we will explore the currently practical unmet needs in inflammation and fibrosis research and clinical practice, as well as fields where urgent progress will be needed in the near future. We welcome submissions covering, but not limited to the following areas:
The mechanisms by which macrophages acquire pro-inflammatory or an-inflammatory lineages and the signaling involved in their transition to these lineages during injury remains a topic of debate. When will TFs be activated to inhibit inflammation or fibrosis? Does overactivation cause inflammation or fibrosis? When does TF activation lead to full restoration and when just to inflammation or fibrosis? Does inhibition of inflammation prevent fibrosis?
Also, DNA methylation can alter TF-DNA binding and function. The association of TFs with each other and with co-activating/repressing proteins are determined by the modular structure of the TFs and the presence of distinct interacting domains. What are the new methylation modifications that have been discovered? What are the new TF binding sites?
Finally, post-translational modifications of TFs by phosphorylation, acetylation, ubiquitination, and nitration can have profound effects on either the DNA-binding capacity or the transcriptional activity of TFs. What are the new post-translational modifications that have been found?
Keywords: transcription factor, inflammation, therapy
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