Glycation-Associated Diabetic Nephropathy and the Role of Long Noncoding RNAs

The glycation of various biomolecules is the root cause of many pathological conditions associated with diabetic nephropathy and end-stage kidney disease. Glycation imbalances metabolism and increases renal cell injury. Numerous therapeutic measures have narrowed down the adverse effects of endogenous glycation, but efficient and potent measures are miles away. Recent advances in the identification and characterization of noncoding RNAs, especially the long noncoding RNAs (lncRNAs), have opened a mammon of new biology to explore the mitigations for glycation-associated diabetic nephropathy. Furthermore, tissue-specific distribution and condition-specific expression make lncRNA a promising key for second-generation therapeutic interventions. Though the techniques to identify and exemplify noncoding RNAs are rapidly evolving, the lncRNA study encounters multiple methodological constraints. This review will discuss lncRNAs and their possible involvement in glycation and advanced glycation end products (AGEs) signaling pathways. We further highlight the possible approaches for lncRNA-based therapeutics and their working mechanism for perturbing glycation and conclude our review with lncRNAs biology-related future opportunities.

Automated summary

The glycation of biomolecules is a major factor in diabetic nephropathy and end-stage kidney disease. Advances in noncoding RNA research, particularly the long noncoding RNAs (lncRNAs), have provided new insights into potential therapies for glycation-related conditions. However, there are still methodological constraints in the study of lncRNAs. This review discusses the role of lncRNAs in glycation and the possible use of lncRNA-based therapeutics.