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Aldosterone/Mineralocorticoid Receptor Downstream Targets as Novel Therapeutic Targets to Prevent Cardiovascular Remodeling

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posted on 22.11.2019 by Jaime Ibarrola, Frederic Jaisser, Natalia López-Andrés

The incidence of heart failure (HF) is increasing because of aging of the population. Despite optimal therapy, patients with HF experience disease progression associated with high mortality rates. HF is still the first cause of hospital admission in subjects aged >65 years. The obvious solution for HF epidemics is to prevent new-onset HF with therapies directed specifically to mechanistic targets that are involved in the transition to HF. The mineralocorticoid receptor (MR) and its natural ligand, the hormone aldosterone (Aldo), play important roles during cardiac and arterial remodeling, but the underlying effects are still not understood. MR antagonists are highly recommended for treatment of systolic symptomatic HF. However, adverse effects limit their use in clinical practice. Galectin-3 (Gal-3), neutrophil gelatinase-associated lipocalin (NGAL), and cardiotrophin-1 (CT-1) have been identified as highly focused targets controlling downstream key MR-mediated HF mechanisms. Therefore, interfering with mechanistic pathways involved in downstream MR activation may provide therapeutic alternatives to MR antagonists. The aim of this review is to focus on the role of the MR biotargets in cardiovascular remodeling.

Funding

IntechOpen

History

Comments

The original book chapter is available at https://www.intechopen.com/ Part of the ‘Aldosterone-Mineralocorticoid Receptor: Cell Biology to Translational Medicine’ collection: https://repository.rcsi.com/account/home#/collections/4974911

Published Citation

Ibarrola J, Jaisser F, López-Andrés. Aldosterone/Mineralocorticoid Receptor Downstream Targets as Novel Therapeutic Targets to Prevent Cardiovascular Remodeling. In: Harvey B, Jaisser F, editors. Aldosterone-Mineralocorticoid Receptor - Cell Biology to Translational Medicine: InTechOpen; 2019.

Publication Date

2019-09-25

Publisher

IntechOpen

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