INTERACTIONS OF RANKL, OSTEOPROTEGERIN AND ADIPOKINES IN REGULATION OF BONE REMODELING IN EXPERIMENTAL CHRONIC KIDNEY

A Goncharova1, S Pavlov1, M Kumetchko1

  • 1Kharkov National Medical University; Kharkov Medical Academy of Postgraduate Education; 3National University of Pharmacy, Ukraine.

Georgian Medical News
|September 12, 2018
PubMed

Insights

This study reveals that chronic kidney disorder in rats alters key cytokines, RANKL, osteoprotegerin, adiponectin, and visfatin, impacting bone-kidney interactions. Adiponectin shows a bone-preserving effect, while visfatin and the RANKL axis exhibit inflammation.

Area of Science:

  • Endocrinology
  • Nephrology
  • Bone Biology

Background:

  • The RANK-RANKL-osteoprotegerin axis is crucial for bone remodeling and bone-kidney interrelations.
  • Adipokines like adiponectin and visfatin are increasingly recognized as regulators in these pathways.
  • Understanding their interplay is vital, especially in conditions like chronic kidney disorder (CKD).

Purpose of the Study:

  • To investigate the roles of the RANK-RANKL-osteoprotegerin axis and the adipokines adiponectin and visfatin in a rat model of CKD.
  • To explore the interrelationships between these key cytokines in the context of CKD.
  • To elucidate the specific effects of these cytokines on bone-kidney interactions during renal impairment.

Main Methods:

  • A chronic kidney disorder model was established in rats 12 weeks post-acute kidney injury induction via glycerol injection.
  • Serum levels of Receptor Activator of Nuclear factor Kappa-B Ligand (RANKL), osteoprotegerin (OPG), adiponectin, and visfatin were quantified using Enzyme-Linked Immunosorbent Assay (ELISA).

Main Results:

  • Rats with CKD exhibited significant increases in RANKL, osteoprotegerin, adiponectin, and visfatin levels.
  • Altered interrelationships among these cytokines were observed in the CKD model.
  • The study identified changes in the cytokine network regulating bone-kidney axis in response to renal dysfunction.

Conclusions:

  • The RANKL-triggered cytokine axis in the bone-kidney network demonstrates an inflammatory character in CKD.
  • Visfatin also contributes to the inflammatory response in this model.
  • Adiponectin appears to exert a protective, bone-preserving effect, counteracting the inflammatory influences.

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