Calcific Aortic Valve Disease-Natural History and Future Therapeutic Strategies.

TAVR aortic valve replacement calcific aortic valve immune system inflammation microbiome severe aortic stenosis

Journal

Frontiers in pharmacology
ISSN: 1663-9812
Titre abrégé: Front Pharmacol
Pays: Switzerland
ID NLM: 101548923

Informations de publication

Date de publication:
2020
Historique:
received: 17 11 2019
accepted: 27 04 2020
entrez: 2 6 2020
pubmed: 2 6 2020
medline: 2 6 2020
Statut: epublish

Résumé

Calcific aortic valve disease (CAVD) is the most frequent heart valve disorder. It is characterized by an active remodeling process accompanied with valve mineralization, that results in a progressive aortic valve narrowing, significant restriction of the valvular area, and impairment of blood flow.The pathophysiology of CAVD is a multifaceted process, involving genetic factors, chronic inflammation, lipid deposition, and valve mineralization. Mineralization is strictly related to the inflammatory process in which both, innate, and adaptive immunity are involved. The underlying pathophysiological pathways that go from inflammation to calcification and, finally lead to severe stenosis, remain, however, incompletely understood. Histopathological studies are limited to patients with severe CAVD and no samples are available for longitudinal studies of disease progression. Therefore, alternative routes should be explored to investigate the pathogenesis and progression of CAVD.Recently, increasing evidence suggests that epigenetic markers such as non-coding RNAs are implicated in the landscape of phenotypical changes occurring in CAVD. Furthermore, the microbiome, an essential player in several diseases, including the cardiovascular ones, has recently been linked to the inflammation process occurring in CAVD. In the present review, we analyze and discuss the CAVD pathophysiology and future therapeutic strategies, focusing on the real and putative role of inflammation, calcification, and microbiome.

Identifiants

pubmed: 32477143
doi: 10.3389/fphar.2020.00685
pmc: PMC7237871
doi:

Types de publication

Journal Article Review

Langues

eng

Pagination

685

Informations de copyright

Copyright © 2020 Alushi, Curini, Christopher, Grubitzch, Landmesser, Amedei and Lauten.

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Auteurs

Brunilda Alushi (B)

Department of Cardiology, Charite´ Universitätsmedizin Berlin and German Centre for Cardiovascular Research (DZHK), Berlin, Germany.
Department of General and Interventional Cardiology, Helios Klinikum Erfurt, Erfurt, Germany.

Lavinia Curini (L)

Department of Cardiology, Charite´ Universitätsmedizin Berlin and German Centre for Cardiovascular Research (DZHK), Berlin, Germany.
Department of Experimental and Clinical Medicine, University of Florence, Firenze, Italy.

Mary Roxana Christopher (MR)

Department of Cardiology, Charite´ Universitätsmedizin Berlin and German Centre for Cardiovascular Research (DZHK), Berlin, Germany.

Herko Grubitzch (H)

Berlin Institute of Health, Berlin, Germany.
Department of Cardiology, German Heart Centre Berlin (DHZB), Berlin, Germany.

Ulf Landmesser (U)

Department of Cardiology, Charite´ Universitätsmedizin Berlin and German Centre for Cardiovascular Research (DZHK), Berlin, Germany.
Berlin Institute of Health, Berlin, Germany.

Amedeo Amedei (A)

Department of Experimental and Clinical Medicine, University of Florence, Firenze, Italy.
Sod of Interdisciplinary Internal Medicine, Azienda Ospedaliera Universitaria Careggi (AOUC), Florence, Italy.

Alexander Lauten (A)

Department of Cardiology, Charite´ Universitätsmedizin Berlin and German Centre for Cardiovascular Research (DZHK), Berlin, Germany.
Department of General and Interventional Cardiology, Helios Klinikum Erfurt, Erfurt, Germany.

Classifications MeSH