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Comment
. 2023 Feb 1;18(2):154-156.
doi: 10.2215/CJN.0000000000000055. Epub 2023 Jan 16.

Concurrent Targeting of Vasopressin Receptor 2 and Somatostatin Receptors in Autosomal Dominant Polycystic Kidney Disease: A Promising Approach for Autosomal Dominant Polycystic Kidney Disease Treatment?

Affiliations
Comment

Concurrent Targeting of Vasopressin Receptor 2 and Somatostatin Receptors in Autosomal Dominant Polycystic Kidney Disease: A Promising Approach for Autosomal Dominant Polycystic Kidney Disease Treatment?

Marie C Hogan et al. Clin J Am Soc Nephrol. .
No abstract available

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Conflict of interest statement

M.C. Hogan reports employment with Mayo Clinic; consultancy agreements with Otsuka Pharmaceuticals; research funding from Camurus, Palladio, Reata, and Regulus Pharmaceuticals; honoraria from American Society of Nephrology; advisory or leadership role for Camurus Pharmaceuticals (no payment), Mayo Clinic Proceedings Quality & Outcomes Journal (no payment), and Sail Bio (no payment); and other interests or relationships with American Society of Nephrology, PKD Disease Outcomes Consortium, and PKD Foundation. T.V. Masyuk reports employment with Mayo Clinic and is an inventor on US Patent 8,232,241 B2 for treating liver diseases.

Figures

Figure 1
Figure 1
In autosomal dominant polycystic kidney disease, mutations in PKD1 or PKD2 gene initiate formation of kidney cysts. Newly formed cysts are characterized by disturbances in multiple cellular pathways, among which cAMP signaling is one of the most important mechanisms underlying progressive cystogenesis. Two cAMP-linked G-protein–coupled receptors, V2R and SSTR, are the major contributors to increased cAMP levels, enhanced fluid secretion, and accelerated cell proliferation in PKD kidneys. Pharmacologic targeting of V2R with tolvaptan and SSTRs with octreotide–long-acting release markedly decrease cAMP production, fluid secretion, and cell proliferation, subsequently inhibiting growth of kidney cysts. cAMP, cyclic adenosine monophosphate; SSTR, somatostatin receptor; V2R, vasopressin receptor 2.

Comment on

References

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