{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T03:47:43Z","timestamp":1792813663303,"version":"4.5.0"},"reference-count":89,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,2,24]],"date-time":"2026-02-24T00:00:00Z","timestamp":1771891200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Endocrinol."],"abstract":"<jats:p>\n                    The cyclic adenosine monophosphate (cAMP)\u2013protein kinase A (PKA) signaling pathway plays a central role in adrenal function, steroidogenesis, and blood pressure regulation. Increasing evidence suggests that dysregulation of this pathway contributes to several forms of hypertension, both endocrine and non-endocrine. A growing number of germline and somatic alterations affecting components of the cAMP\/PKA axis have been implicated as key drivers of hypertensive disorders. Among these, activating pathogenic variants (PV) in\n                    <jats:italic>GNAS<\/jats:italic>\n                    , which encodes the stimulatory G protein \u03b1-subunit (Gs\u03b1) responsible for cAMP production, have been linked to cortisol excess. Mosaic\n                    <jats:italic>GNAS<\/jats:italic>\n                    PV\n                    <jats:italic>cause McCune-Albright syndrome<\/jats:italic>\n                    , which may present with ACTH-independent Cushing syndrome, while somatic\n                    <jats:italic>GNAS<\/jats:italic>\n                    PV have been identified in cortisol-producing adrenal adenomas. Germline inactivating variants in\n                    <jats:italic>PRKAR1A<\/jats:italic>\n                    are associated with\n                    <jats:italic>Carney complex and primary pigmented nodular adrenocortical disease (PPNAD).<\/jats:italic>\n                    Furthermore, germline alterations in phosphodiesterases such as\n                    <jats:italic>PDE11A<\/jats:italic>\n                    and\n                    <jats:italic>PDE8B<\/jats:italic>\n                    , which impair cAMP degradation, have been associated with Cushing syndrome and micronodular adrenal hyperplasia. Somatic activating PV in\n                    <jats:italic>PRKACA<\/jats:italic>\n                    , the gene encoding the catalytic subunit of PKA, have also been described in cortisol-producing adenomas. In primary aldosteronism, recent studies\u2014including data from our group\u2014suggest that germline variants in\n                    <jats:italic>PDE2A<\/jats:italic>\n                    and\n                    <jats:italic>PDE3B<\/jats:italic>\n                    may contribute to bilateral adrenal hyperplasia and autonomous aldosterone production by modulating intracellular cAMP levels. Additionally, gain-of-function PV in\n                    <jats:italic>PDE3A<\/jats:italic>\n                    have been associated with a familial form of salt-independent hypertension characterized by enhanced PKA signaling and vascular remodeling. This expanding body of evidence underscores the critical role of the cAMP\/PKA pathway in the pathophysiology of distinct hypertensive phenotypes and highlights novel molecular mechanisms and potential therapeutic targets that merit further investigation.\n                  <\/jats:p>","DOI":"10.3389\/fendo.2026.1748702","type":"journal-article","created":{"date-parts":[[2026,2,24]],"date-time":"2026-02-24T05:18:57Z","timestamp":1771910337000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":3,"title":["cAMP\/PKA signaling in endocrine hypertension: genetic mechanisms and pathophysiological insights"],"prefix":"10.3389","volume":"17","author":[{"given":"Jose Antonio B.","family":"Lima Sobrinho","sequence":"first","affiliation":[{"name":"Unidade de Adrenal, Laborat\u00f3rio de Endocrinologia Molecular e Celular Laborat\u00f3rio de Investiga\u00e7\u00e3o M\u00e9dica 25' (LIM25), Divis\u00e3o de Endocrinologia e Metabologia, Hospital das Cl\u00ednicas, Faculdade de Medicina da Universidade de S\u00e3o Paulo","place":["S\u00e3o Paulo, Brazil"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Madson Q.","family":"Almeida","sequence":"additional","affiliation":[{"name":"Unidade de Adrenal, Laborat\u00f3rio de Endocrinologia Molecular e Celular Laborat\u00f3rio de Investiga\u00e7\u00e3o M\u00e9dica 25' (LIM25), Divis\u00e3o de Endocrinologia e Metabologia, Hospital das Cl\u00ednicas, Faculdade de Medicina da Universidade de S\u00e3o Paulo","place":["S\u00e3o Paulo, Brazil"]},{"name":"Unidade de Oncologia End\u00f3crina, Instituto do C\u00e2ncer do Estado de S\u00e3o Paulo (ICESP), Faculdade de Medicina da Universidade de S\u00e3o Paulo","place":["S\u00e3o Paulo, 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