{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T16:56:48Z","timestamp":1789923408450,"version":"4.0.1"},"reference-count":99,"publisher":"Bioscientifica","issue":"2","content-domain":{"domain":["joe.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2015,2]]},"abstract":"<jats:p>\n                    Primary aldosteronism (PA) is the most common and curable form of secondary hypertension. It is caused in the majority of cases by either unilateral aldosterone overproduction due to an aldosterone-producing adenoma (APA) or by bilateral adrenal hyperplasia. Recent advances in genome technology have allowed researchers to unravel part of the genetic abnormalities underlying the development of APA and familial hyperaldosteronism. Recurrent somatic mutations in genes coding for ion channels (\n                    <jats:italic>KCNJ5<\/jats:italic>\n                    and\n                    <jats:italic>CACNA1D<\/jats:italic>\n                    ) and ATPases (\n                    <jats:italic>ATP1A1<\/jats:italic>\n                    and\n                    <jats:italic>ATP2B3<\/jats:italic>\n                    ) regulating intracellular ionic homeostasis and cell membrane potential have been identified in APA. Similar germline mutations of\n                    <jats:italic>KCNJ5<\/jats:italic>\n                    were identified in a severe familial form of PA, familial hyperaldosteronism type 3 (FH3), whereas\n                    <jats:italic>de novo<\/jats:italic>\n                    germline\n                    <jats:italic>CACNA1D<\/jats:italic>\n                    mutations were found in two cases of hyperaldosteronism associated with a complex neurological disorder. These results have allowed a pathophysiological model of APA development to be established. This model involves modifications in intracellular ionic homeostasis and membrane potential, accounting for \u223c50% of all tumors, associated with specific gender differences and severity of PA. In this review, we describe the different genetic abnormalities associated with PA and discuss the mechanisms whereby they lead to increased aldosterone production and cell proliferation. We also address some of the foreseeable consequences that genetic knowledge may contribute to improve diagnosis and patient care.\n                  <\/jats:p>","DOI":"10.1530\/joe-14-0597","type":"journal-article","created":{"date-parts":[[2014,11,26]],"date-time":"2014-11-26T00:52:30Z","timestamp":1416963150000},"page":"R63-R77","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-1","source":"Crossref","is-referenced-by-count":55,"title":["An update on novel mechanisms of primary aldosteronism"],"prefix":"10.1530","volume":"224","author":[{"given":"Maria-Christina","family":"Zennaro","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sheerazed","family":"Boulkroun","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fabio","family":"Fernandes-Rosa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","reference":[{"key":"1_49540714","doi-asserted-by":"crossref","first-page":"138","DOI":"10.1159\/000358197","volume":"82","year":"2014","journal-title":"HORMONE RESEARCH IN PADIATRICS"},{"key":"2_45944666","doi-asserted-by":"crossref","first-page":"1117","DOI":"10.1161\/HYPERTENSIONAHA.110.168740","volume":"57","year":"2011","journal-title":"OCL Hypertension"},{"issue":"7","key":"3_43336849","doi-asserted-by":"publisher","first-page":"e41926","DOI":"10.1371\/journal.pone.0041926","volume":"7","author":"Akerstrom","year":"2012","ISSN":"https:\/\/id.crossref.org\/issn\/1932-6203","issn-type":"print"},{"issue":"4","key":"4_41002294","doi-asserted-by":"publisher","first-page":"419","DOI":"10.1007\/s00380-011-0191-8","volume":"27","author":"Aritomi","year":"2012","journal-title":"Heart and vessels","ISSN":"https:\/\/id.crossref.org\/issn\/0910-8327","issn-type":"print"},{"issue":"5","key":"5_42208575","doi-asserted-by":"publisher","first-page":"E819","DOI":"10.1210\/jc.2011-2965","volume":"97","year":"2012","journal-title":"Journal of Clinical Endocrinology &amp; Metabolism","ISSN":"https:\/\/id.crossref.org\/issn\/0021-972X","issn-type":"print"},{"key":"6_46521413","doi-asserted-by":"crossref","first-page":"1055","DOI":"10.1038\/ng.2716","volume":"45","year":"2013","journal-title":"Nature genetics","ISSN":"https:\/\/id.crossref.org\/issn\/1061-4036","issn-type":"print"},{"key":"7_49540715","doi-asserted-by":"crossref","first-page":"582","DOI":"10.1111\/j.1440-1681.1996.tb02786.x","volume":"23","year":"1996","journal-title":"CLINICAL AND EXPERIMENTAL PHARMACOLOGY PHYSIOLOGY"},{"key":"8_45944669","doi-asserted-by":"crossref","first-page":"584","DOI":"10.1111\/j.1440-1681.1996.tb02787.x","volume":"23","year":"1996","journal-title":"CLINICAL AND EXPERIMENTAL PHARMACOLOGY PHYSIOLOGY"},{"issue":"6","key":"9_36347500","doi-asserted-by":"publisher","first-page":"450","DOI":"10.1055\/s-0029-1243601","volume":"42","author":"Bandulik","year":"2010","journal-title":"Hormone and metabolic research. 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