Abstract
It has been well established that the etiopathogenesis of diverse autoimmune diseases is rooted in the autoreactive immune cells’ excessively proliferative state and impaired apoptotic machinery. Survivin is an anti-apoptotic and mitotic factor that has sparked a considerable research interest in this field. Survivin overexpression has been shown to contribute significantly to the development of autoimmune diseases via autoreactive immune cell overproliferation and apoptotic dysregulation. Several microRNAs (miRNAs/miRs) have been discovered to be involved in survivin regulation, rendering the survivin-miRNA axis a perspective target for autoimmune disease therapy. In this review, we discuss the role of survivin as an immune regulator and a highly implicated protein in the pathogenesis of autoimmune diseases, the significance of survivin-targeting miRNAs in autoimmunity, and the feasibility of targeting the survivin-miRNA axis as a promising therapeutic option for autoimmune diseases.
Highlights
The complex etiopathogenesis of various autoimmune conditions has prompted researchers to investigate the molecular basis and factors associated with the high proliferative and apoptosisresistant state of implicated cells [1, 2]
Survivin overexpression in autoimmune disease contributes to escape apoptosis in autoreactive B cells, preserving autoreactive lymphocytes that would otherwise be eliminated by apoptosis [41]. These findings indicate that survivin has the potential to be a therapeutic target in autoimmune diseases [42]
In vitro studies revealed that overexpression of miR-20a-3p directly induces post-transcriptional suppression of SFMBT1, leading to transforming growth factor beta-1 (TGFb1) and P-smad2/3 protein upregulation and survivin downregulation [67]
Summary
The complex etiopathogenesis of various autoimmune conditions has prompted researchers to investigate the molecular basis and factors associated with the high proliferative and apoptosisresistant state of implicated cells [1, 2]. Multiple survivinspecific miRNAs with aberrant expression profiles have been identified in autoimmune diseases that play a central role in survivin regulation (Table 1). Other miRNAs with dysregulated expression patterns in RA patients, such as miR-335 and miR485, have been identified to regulate survivin through direct interaction with its mRNA [7, 74, 94].
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