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The inflammation-related microRNA network, often referred to as "inflammamiRs," is a complex regulatory system of small non-coding RNAs that fine-tune the expression of genes involved in the immune response. Key members of this network, such as miR-155, miR-146a, and miR-21, act as post-transcriptional rheostats that modulate critical signaling pathways, including NF-κB, TLR, and JAK/STAT (Source: Quinn and O'Neill, 2011). By binding to the 3' untranslated regions of target mRNAs, these microRNAs control the production of pro-inflammatory cytokines and the activation state of immune cells like macrophages and T cells (Source: O'Connell et al., 2012). Dysregulation of this network is a central feature of chronic inflammatory diseases, autoimmune disorders, and certain cancers, where it contributes to persistent inflammation and tissue damage. Therapeutic strategies targeting this network do not address the network as a single entity but rather focus on modulating specific microRNA components to restore homeostatic balance. For example, the drug Cobomarsen is an antisense oligonucleotide designed to inhibit miR-155 in patients with lymphoma and chronic inflammation (Source: Blood, 2020). Other approaches include the use of miRNA mimics, such as Remlarsen for miR-29, to counteract fibrosis by replacing deficient anti-inflammatory or anti-fibrotic signals (Source: Nature Reviews Drug Discovery, 2017). Despite the promise of these therapies, significant challenges remain, particularly regarding the delivery of RNA molecules to specific tissues and the potential for off-target effects due to the multi-target nature of microRNAs (Source: Molecular Therapy, 2019).
Antisense inhibition of pro-inflammatory microRNAs or replacement of anti-inflammatory microRNAs to modulate gene expression within immune signaling pathways (Source: Nature Reviews Drug Discovery, 2017).
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