{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,22]],"date-time":"2026-07-22T19:52:33Z","timestamp":1784749953010,"version":"3.55.0"},"reference-count":135,"publisher":"MDPI AG","issue":"17","license":[{"start":{"date-parts":[[2024,8,30]],"date-time":"2024-08-30T00:00:00Z","timestamp":1724976000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Chronic kidney disease (CKD) is characterized by a steady decline in kidney function and affects roughly 10% of the world\u2019s population. This review focuses on the critical function of cyclic adenosine monophosphate (cAMP) signaling in CKD, specifically how it influences both protective and pathogenic processes in the kidney. cAMP, a critical secondary messenger, controls a variety of cellular functions, including transcription, metabolism, mitochondrial homeostasis, cell proliferation, and apoptosis. Its compartmentalization inside cellular microdomains ensures accurate signaling. In kidney physiology, cAMP is required for hormone-regulated activities, particularly in the collecting duct, where it promotes water reabsorption through vasopressin signaling. Several illnesses, including Fabry disease, renal cell carcinoma, nephrogenic diabetes insipidus, Bartter syndrome, Liddle syndrome, diabetic nephropathy, autosomal dominant polycystic kidney disease, and renal tubular acidosis, have been linked to dysfunction in the cAMP system. Both cAMP analogs and phosphodiesterase inhibitors have the potential to improve kidney function and reduce kidney damage. Future research should focus on developing targeted PDE inhibitors for the treatment of CKD.<\/jats:p>","DOI":"10.3390\/ijms25179441","type":"journal-article","created":{"date-parts":[[2024,8,30]],"date-time":"2024-08-30T09:39:32Z","timestamp":1725010772000},"page":"9441","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Cyclic Adenosine Monophosphate Signaling in Chronic Kidney Disease: Molecular Targets and Therapeutic Potentials"],"prefix":"10.3390","volume":"25","author":[{"given":"Charlotte","family":"Delrue","sequence":"first","affiliation":[{"name":"Department of Nephrology, Ghent University Hospital, 9000 Ghent, Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9421-3546","authenticated-orcid":false,"given":"Reinhart","family":"Speeckaert","sequence":"additional","affiliation":[{"name":"Department of Dermatology, Ghent University Hospital, 9000 Ghent, Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3072-5080","authenticated-orcid":false,"given":"Rafael Noal","family":"Moresco","sequence":"additional","affiliation":[{"name":"Graduate Program in Pharmaceutical Sciences, Center of Health Sciences, Federal University of Santa Maria, Santa Maria 97105-900, Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9183-4390","authenticated-orcid":false,"given":"Marijn M.","family":"Speeckaert","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Ghent University Hospital, 9000 Ghent, Belgium"},{"name":"Research Foundation-Flanders (FWO), 1000 Brussels, Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2024,8,30]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","unstructured":"Fularski, P., Czarnik, W., Frankenstein, H., G\u0105sior, M., M\u0142ynarska, E., Rysz, J., and Franczyk, B. 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