Urolithiasis is a multifactorial metabolic disease caused by the interaction of genetic and environmental factors. Today, the
study of urolithiasis is a hot topic due to the steady increase in both incidence and prevalence, as well as the high recurrence rate of
this disease. In urolithiasis, the majority of concrements are forming on the base of calcium salts. The study of the molecular and
genetic aspects of hypercalciuria is a promising way to improve urolithiasis control. Claudins are the proteins of renal epithelium
tight junctions that play an important role in the calcium reabsorption in kidney.
In this review, we describe actual worldwide data on the epigenetic regulation of kidney claudins activity via small noncoding
RNAs and the perspectives of using “claudins – microRNA” system components for the urolithiasis targeted pharmacotherapy. The
article contains information on the segment-specific expression of claudins in nephrons, claudinopathies associated with impaired
calcium metabolism in the kidneys, tight junctions as dynamic equilibrium systems, microRNA biogenesis and principles of action,
various therapeutic strategies using microRNAs.