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Biomedicines
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Recent Advances in Primary Aldosteronism: From Bench to Clinic
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Recent Advances in Primary Aldosteronism: From Bench to Clinic

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Endocrinology and Metabolism Research".

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 4462

Special Issue Editor

Prof. Dr. Yen-Hung Lin

E-Mail Website
Guest Editor
Department of Internal Medicine, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei 100, Taiwan
Interests: aldosterone; mineralocorticoid receptor; heart failure; pulmonary hypertension; heart rhythm complexity

Special Issue Information

Dear Colleagues,

Primary aldosteronism (PA) is the most important cause of secondary hypertension. Its prevalence is about 5 to 10% in all hypertensive patients. PA is characterized by its excessive endogenous aldosterone production which causes more cardiovascular complications, including coronary artery disease, myocardial infarction, stroke, atrial fibrillation, and heart failure. In addition, PA patients also had higher incidence of renal disease, metabolic disorders, bone disease, mental disorders, and immune system disorders. Early diagnosis and timely treatment are crucial to prevent deleterious cardiovascular outcomes and other systemic complications. In the past decade, the discovery of genetic abnormalities, responsible for sporadic and familial forms of PA, subtypes of concurrent cortisol secretion, its effects of on cardiovascular remodeling, and the development of treatment options, have improved the knowledge of this disease.

However, our understanding of the basic aspects of the pathophysiology of this disease, establishing the best diagnostic methods, linkage of aldosterone to the target-organ complications, and the long-term treatment effects to these patients, are still incomplete.

With this Special Issue in Biomedicines, we aim to present a journal on the actual state of the art in order to understand the pathophysiology of PA, different subtypes of genetic abnormalities or concurrent hypercortisolism, the effects of excess aldosterone on other organ/systems, and the treatments of PA (from bench to clinic). We welcomed the submission of review and original research articles (clinical or basic) regarding pathophysiology, clinical implications, as well as the diagnosis and treatment of PA.

Prof. Dr. Yen-Hung Lin
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • primary aldosteronism
  • aldosterone
  • renin
  • mineralocorticoid receptor
  • somatic mitation
  • hypercortisolism
  • cardiovascular
  • remodeling

Published Papers (2 papers)

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Research

13 pages, 1286 KiB  
Article
High Prevalence of Primary Aldosteronism in Patients with Type 2 Diabetes Mellitus and Hypertension
by Ernestini Tyfoxylou, Nick Voulgaris, Chris Gravvanis, Sophia Vlachou, Athina Markou, Labrini Papanastasiou, Nikolaos Tentolouris, Eva Kassi, Gregory Kaltsas, George P. Chrousos and George P. Piaditis
Biomedicines 2022, 10(9), 2308; https://doi.org/10.3390/biomedicines10092308 - 16 Sep 2022
Cited by 2 | Viewed by 1675
Abstract
Primary aldosteronism (PA) is the most common cause of endocrine hypertension. The prevalence of hypertension is higher in patients with diabetes mellitus-2 (DM-2). Following the limited existing data, we prospectively investigated the prevalence of aldosterone excess either as autonomous secretion (PA) or as [...] Read more.
Primary aldosteronism (PA) is the most common cause of endocrine hypertension. The prevalence of hypertension is higher in patients with diabetes mellitus-2 (DM-2). Following the limited existing data, we prospectively investigated the prevalence of aldosterone excess either as autonomous secretion (PA) or as a hyper-response to stress in hypertensive patients with DM-2 (HDM-2). A total of 137 HDM-2 patients and 61 non-diabetics with essential hypertension who served as controls (EH-C) underwent a combined, overnight diagnostic test, the Dexamethasone–captopril–valsartan test (DCVT) used for the diagnosis of PA and an ultralow dose (0.3 μg) ACTH stimulation test to identify an exaggerated aldosterone response to ACTH stimulation. Twenty-three normotensive individuals served as controls (NC) to define the normal response of aldosterone (ALD) and aldosterone-to-renin ratio (ARR) to the ultralow dose ACTH test. Using post-DCVTALD and ARR from the EH-C, and post-ACTH peak ALD and ARR from the NC, 47 (34.3%) HDM-2 patients were found to have PA, whereas 6 (10.4%) HDM-2 patients without PA (DCVT-negative) exhibited an exaggerated aldosterone response to stress—a prevalence much higher than ever reported. Treatment with mineralocorticoid receptor antagonists (MRAs) induced a significant and permanent reduction of BP in all HDM-2 patients. Early diagnosis and targeted treatment of PA is crucial to prevent any aggravating effect on chronic diabetic complications. Full article
(This article belongs to the Special Issue Recent Advances in Primary Aldosteronism: From Bench to Clinic)
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12 pages, 3348 KiB  
Article
Aldosterone Suppresses Endothelial Mitochondria through Mineralocorticoid Receptor/Mitochondrial Reactive Oxygen Species Pathway
by Shih-Yuan Peng, Cheng-Hsuan Tsai, Xue-Ming Wu, Hsin-Hsiu Huang, Zheng-Wei Chen, Bo-Ching Lee, Yi-Yao Chang, Chien-Ting Pan, Vin-Cent Wu, Chia-Hung Chou, Chi-Sheng Hung, Che-Wei Liao and Yen-Hung Lin
Biomedicines 2022, 10(5), 1119; https://doi.org/10.3390/biomedicines10051119 - 12 May 2022
Cited by 4 | Viewed by 2181
Abstract
Excessive aldosterone secretion causes endothelial dysfunction, vascular inflammation, and vascular fibrosis in patients with primary aldosteronism (PA). Endothelial function is closely related to endothelial mitochondria. However, the effects of elevated aldosterone levels on endothelial mitochondria remain unclear. In this study, we used primary [...] Read more.
Excessive aldosterone secretion causes endothelial dysfunction, vascular inflammation, and vascular fibrosis in patients with primary aldosteronism (PA). Endothelial function is closely related to endothelial mitochondria. However, the effects of elevated aldosterone levels on endothelial mitochondria remain unclear. In this study, we used primary cultured human umbilical vein endothelial cells (HUVECs) to investigate the effects of aldosterone on endothelial mitochondria. Mineralocorticoid receptor (MR) small interfering (si)RNA or glucocorticoid receptor (GR) siRNA were used to confirm the pathway by which aldosterone exerts its effects on the mitochondria of HUVECs. The results showed that excess aldosterone suppressed mitochondrial DNA copy numbers, anti-mitochondrial protein, and SOD2 protein expression in a dose- and time-dependent manner. These effects were attenuated by treatment with MR siRNA, but not with GR siRNA. Furthermore, it was attenuated by treatment with a mitochondria-targeted antioxidant (Mito-TEMPO, associated with mitochondrial reactive oxygen species (ROS) production), but not N-acetyl-L-cysteine (associated with cytosolic ROS production), which suggests that the process was through the mitochondrial ROS pathway, but not the cytosolic ROS pathway. In conclusion, aldosterone excess suppressed endothelial mitochondria through the MR/mitochondrial ROS pathway. Full article
(This article belongs to the Special Issue Recent Advances in Primary Aldosteronism: From Bench to Clinic)
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