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Palmitic acid regulated anti-inflammatory lncRNA (PARAIL) is a long noncoding RNA induced by palmitic acid, cytokines, and infectious agents in monocytes and macrophages[1]. It is upregulated during the resolution phase of inflammation and functions by interacting with RNA-binding proteins, notably ELAVL1, to modulate the stability and expression of inflammatory genes. Knockdown of PARAIL leads to increased pro-inflammatory gene expression, while overexpression attenuates inflammation. Mouse orthologs of PARAIL are downregulated in diabetic and atherosclerotic conditions, linking its expression to metabolic disease progression[1]. It is also implicated in cancer biology, as high expression correlates with poor prognosis in colorectal cancer and is associated with immune cell infiltration and immune checkpoint gene expression[3][4]. PARAIL represents a novel therapeutic target for diseases driven by chronic inflammation and immune dysregulation[1][3][4].
Modulation of PARAIL expression or function Antisense oligonucleotides or lncRNA mimics could theoretically be used to enhance or suppress PARAIL function, influencing pro- or anti-inflammatory gene expression
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