Key result
Aldosterone-producing adenomas show distinct transcriptomic and metabolomic profiles driven primarily by KCNJ5 mutational status.
Why the study?
Understanding the pathophysiological background of primary aldosteronism is important to provide ameliorative treatment strategies, with significant recent progress in clarifying the genetic and molecular mechanisms of aldosterone-producing adenomas.
Systematic Review
Understanding the distinct molecular and metabolic profiles of primary aldosteronism subtypes could contribute to the development of personalized treatments.
Answers are grounded in this paper and cite their sources.
May inform mutation-specific therapies in primary aldosteronism; extends molecular profiling of aldosterone-producing adenomas beyond known somatic mutations.
Introduction: Primary aldosteronism (PA) is the most common cause of endocrine hypertension, mainly caused by aldosterone-producing adenomas or hyperplasia; understanding its pathophysiological background is important in order to provide ameliorative treatment strategies. Over the past several years, significant progress has been documented in this field, in particular in the clarification of the genetic and molecular mechanisms responsible for the pathogenesis of aldosterone-producing adenomas (APAs). Methods: Systematic searches of the PubMed and Cochrane databases were performed for all human studies applying transcriptomic, epigenetic or metabolomic analyses to PA subjects. Studies involving serial analysis of gene expression and microarray, epigenetic studies with methylome analyses and micro-RNA expression profiles, and metabolomic studies focused on improving understanding of the regulation of autonomous aldosterone production in PA were all included. Results: In this review we summarize the main findings in this area and analyze the interplay between primary aldosteronism and several signaling pathways with differential regulation of the RNA and protein expression of several factors involved in, among others, steroidogenesis, calcium signaling, and nuclear, membrane and G-coupled protein receptors. Distinct transcriptomic and metabolomic patterns are also presented herein, depending on the mutational status of APAs. In particular, two partially opposite transcriptional and steroidogenic profiles appear to distinguish APAs carrying a KCNJ5 mutation from all other APAs, which carry different mutations. Conclusions: These findings can substantially contribute to the development of personalized treatment in patients with PA.
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Spyroglou et al. (2021) conducted a systematic review in Primary Aldosteronism. Transcriptomic, epigenetic, and metabolomic profiling was evaluated. Aldosterone-producing adenomas exhibit distinct transcriptomic and metabolomic patterns that depend on their mutational status, particularly distinguishing KCNJ5 mutations from other mutations.
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