Aldosterone and Mineralocorticoid Receptor System in Cardiovascular Physiology and Pathophysiology
The mineralocorticoid hormone aldosterone (Aldo) has been intensively studied for its ability to influence both the physiology and pathophysiology of the cardiovascular system. Indeed, although research on Aldo actions for decades has mainly focused on its effects in the kidney, several lines of evidence have now demonstrated that this hormone exerts disparate extrarenal adverse effects, especially in the circulatory system. Accordingly, in the last lusters, a number of studies in preclinical models (in vitro and in vivo) and in humans have established that Aldo, following the interaction with its receptor-the mineralocorticoid receptor (MR)-is able to activate specific intracellular genomic and nongenomic pathways, thus regulating the homeostasis of the cardiovascular system. Importantly, through this mechanism of action, this hormone becomes a crucial regulator of the function and growth of different types of cells, including fibroblasts, cardiomyocytes, and vascular cells. For this main reason, it is plausible that when Aldo is present at high levels in the blood, it profoundly modifies the physiology of these cells, therefore being at the foundation of several cardiovascular disorders, such as heart failure (HF). On these grounds, in this review, we will provide an updated account on the current knowledge concerning Aldo activity in the cardiovascular system and the most recent preclinical studies and clinical trials designed to test better approaches able to counter the hyperactivity of the Aldo/MR signaling pathway in the setting of cardiovascular diseases.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2018 |
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| Erschienen: |
2018 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:2018 |
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| Enthalten in: |
Oxidative medicine and cellular longevity - 2018(2018) vom: 16., Seite 1204598 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Cannavo, Alessandro [VerfasserIn] |
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| Links: |
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| Themen: |
4964P6T9RB |
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| Anmerkungen: |
Date Completed 11.12.2018 Date Revised 16.11.2019 published: Electronic-eCollection Citation Status MEDLINE |
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| doi: |
10.1155/2018/1204598 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM289624347 |
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| 520 | |a The mineralocorticoid hormone aldosterone (Aldo) has been intensively studied for its ability to influence both the physiology and pathophysiology of the cardiovascular system. Indeed, although research on Aldo actions for decades has mainly focused on its effects in the kidney, several lines of evidence have now demonstrated that this hormone exerts disparate extrarenal adverse effects, especially in the circulatory system. Accordingly, in the last lusters, a number of studies in preclinical models (in vitro and in vivo) and in humans have established that Aldo, following the interaction with its receptor-the mineralocorticoid receptor (MR)-is able to activate specific intracellular genomic and nongenomic pathways, thus regulating the homeostasis of the cardiovascular system. Importantly, through this mechanism of action, this hormone becomes a crucial regulator of the function and growth of different types of cells, including fibroblasts, cardiomyocytes, and vascular cells. For this main reason, it is plausible that when Aldo is present at high levels in the blood, it profoundly modifies the physiology of these cells, therefore being at the foundation of several cardiovascular disorders, such as heart failure (HF). On these grounds, in this review, we will provide an updated account on the current knowledge concerning Aldo activity in the cardiovascular system and the most recent preclinical studies and clinical trials designed to test better approaches able to counter the hyperactivity of the Aldo/MR signaling pathway in the setting of cardiovascular diseases | ||
| 650 | 4 | |a Journal Article | |
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| 650 | 7 | |a Aldosterone |2 NLM | |
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| 700 | 1 | |a Bencivenga, Leonardo |e verfasserin |4 aut | |
| 700 | 1 | |a Liccardo, Daniela |e verfasserin |4 aut | |
| 700 | 1 | |a Elia, Andrea |e verfasserin |4 aut | |
| 700 | 1 | |a Marzano, Federica |e verfasserin |4 aut | |
| 700 | 1 | |a Gambino, Giuseppina |e verfasserin |4 aut | |
| 700 | 1 | |a D'Amico, Maria Loreta |e verfasserin |4 aut | |
| 700 | 1 | |a Perna, Claudia |e verfasserin |4 aut | |
| 700 | 1 | |a Ferrara, Nicola |e verfasserin |4 aut | |
| 700 | 1 | |a Rengo, Giuseppe |e verfasserin |4 aut | |
| 700 | 1 | |a Paolocci, Nazareno |e verfasserin |4 aut | |
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