Abstract
This review focuses on Receptor for Advanced Glycation Endproducts/Diaphonous related formin1 (RAGE/Diaph1) interaction as a modulator of actin cytoskeleton dynamics in peripheral nervous system (PNS) in diabetes. Deciphering the complex molecular interactions between RAGE and Diaph1 is crucial in expanding our understanding of diabetic length dependent neuropathy (DLDN). DLDN is a common neurological disorder in patients with diabetes. It is well known that actin cytoskeletal homeostasis is disturbed during DLDN. Thus, we review the current status of knowledge about RAGE/Diaph1 impact on actin cytoskeletal malfunctions in PNS and DLDN progression in diabetes. We also survey studies about small molecules that may block RAGE/Diaph1 axis and thus inhibit the progression of DLDN. Finally, we explore examples of cytoskeletal long-non coding RNAs (lncRNAs) currently unrelated to DLDN, to discuss their potential role in this disease. Most recent studies indicated that lncRNAs have a great potential in many research areas, including RAGE/Diaph1 axis as well as DLDN. Altogether, this review is aimed at giving us an insight into the involvement of cytoskeletal lncRNAs in DLDN.
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