TY - JOUR
T1 - Dissecting the molecular pathways of primary aldosteronism
AU - Nakamura, Yasuhiro
AU - Felizola, Saulo J.A.
AU - Satoh, Fumitoshi
AU - Konosu-Fukaya, Sachiko
AU - Sasano, Hironobu
N1 - Publisher Copyright:
© 2014 Japanese Society of Pathology and Wiley Publishing Asia Pty Ltd.
PY - 2014/10/1
Y1 - 2014/10/1
N2 - The great majority of the cases clinically diagnosed as primary aldosteronism (PA) have been caused by aldosterone-producing adenoma (APA) or idiopathic hyperaldosteronism (IHA). The differential diagnosis of both subtypes of PA 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 PA including the aberrant expression of G-protein coupled receptors (GPCRs), 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 PA. These novel findings indicate that the molecular mechanisms on the onset and pathophysiology of PA are more complicated than previously considered and further clarification of clinical relevance of these findings is required at this juncture.
AB - The great majority of the cases clinically diagnosed as primary aldosteronism (PA) have been caused by aldosterone-producing adenoma (APA) or idiopathic hyperaldosteronism (IHA). The differential diagnosis of both subtypes of PA 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 PA including the aberrant expression of G-protein coupled receptors (GPCRs), 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 PA. These novel findings indicate that the molecular mechanisms on the onset and pathophysiology of PA are more complicated than previously considered and further clarification of clinical relevance of these findings is required at this juncture.
KW - Ca signaling pathway
KW - G-protein coupled receptor
KW - Primary aldosteronism
KW - Somatic mutation
KW - Steroidogenic enzymes
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U2 - 10.1111/pin.12200
DO - 10.1111/pin.12200
M3 - Article
C2 - 25274410
AN - SCOPUS:84937511257
VL - 64
SP - 482
EP - 489
JO - Acta Pathologica Japonica
JF - Acta Pathologica Japonica
SN - 1320-5463
IS - 10
ER -