{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T01:15:18Z","timestamp":1790039718757,"version":"4.0.1"},"reference-count":50,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2014,10,2]],"date-time":"2014-10-02T00:00:00Z","timestamp":1412208000000},"content-version":"vor","delay-in-days":1,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100007449","name":"Takeda Science Foundation","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100007449","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Pathology International"],"published-print":{"date-parts":[[2014,10]]},"abstract":"<jats:p>\n                    The great majority of the cases clinically diagnosed as primary aldosteronism (\n                    <jats:styled-content style=\"fixed-case\">PA<\/jats:styled-content>\n                    ) have been caused by aldosterone\u2010producing adenoma (\n                    <jats:styled-content style=\"fixed-case\">APA<\/jats:styled-content>\n                    ) or idiopathic hyperaldosteronism (\n                    <jats:styled-content style=\"fixed-case\">IHA<\/jats:styled-content>\n                    ). The differential diagnosis of both subtypes of\n                    <jats:styled-content style=\"fixed-case\">PA<\/jats:styled-content>\n                    is important due to the different therapeutic modes but clinically it is sometimes difficult. It is also important to understand the morphological features of these two subtypes with special emphasis upon differences of the status for aldosterone biosynthesis. In the last decade, molecular mechanisms of\n                    <jats:styled-content style=\"fixed-case\">PA<\/jats:styled-content>\n                    including the aberrant expression of\n                    <jats:styled-content style=\"fixed-case\">G<\/jats:styled-content>\n                    \u2010protein coupled receptors (\n                    <jats:styled-content style=\"fixed-case\">GPCR<\/jats:styled-content>\n                    s), key regulators of the intracellular calcium signaling pathway and somatic mutations of ion channels, have been revealed and our understanding of the molecular pathways involved in excessive aldosterone production has been markedly advanced. In addition, newly developed monoclonal antibodies specific to the isoform of adrenal steroidogenic enzymes have demonstrated the novel profiles of adrenal steroidogenesis in\n                    <jats:styled-content style=\"fixed-case\">PA<\/jats:styled-content>\n                    . These novel findings indicate that the molecular mechanisms on the onset and pathophysiology of\n                    <jats:styled-content style=\"fixed-case\">PA<\/jats:styled-content>\n                    are more complicated than previously considered and further clarification of clinical relevance of these findings is required at this juncture.\n                  <\/jats:p>","DOI":"10.1111\/pin.12200","type":"journal-article","created":{"date-parts":[[2014,10,2]],"date-time":"2014-10-02T03:59:34Z","timestamp":1412222374000},"page":"482-489","source":"Crossref","is-referenced-by-count":20,"title":["Dissecting the molecular pathways of primary aldosteronism"],"prefix":"10.1111","volume":"64","author":[{"given":"Yasuhiro","family":"Nakamura","sequence":"first","affiliation":[{"name":"Department of Pathology Tohoku University Graduate School of Medicine  Sendai Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Saulo J.A.","family":"Felizola","sequence":"additional","affiliation":[{"name":"Department of Pathology Tohoku University Graduate School of Medicine  Sendai Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fumitoshi","family":"Satoh","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Endocrinology, and Vascular Medicine Tohoku University Hospital  Sendai Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sachiko","family":"Konosu\u2010Fukaya","sequence":"additional","affiliation":[{"name":"Department of Pathology Tohoku University Graduate School of Medicine  Sendai Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hironobu","family":"Sasano","sequence":"additional","affiliation":[{"name":"Department of Pathology Tohoku University Graduate School of Medicine  Sendai Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2014,10,2]]},"reference":[{"key":"e_1_2_10_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2005.01.015"},{"key":"e_1_2_10_3_1","first-page":"211","volume-title":"Adrenal Cortex. 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