Calcific Aortic Valve Stenosis: Methods, Models, and Mechanisms

Jordan D Miller; Robert M Weiss; Donald D Heistad

doi:10.1161/CIRCRESAHA.110.234138

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Calcific Aortic Valve Stenosis: Methods, Models, and Mechanisms

Journal article

Open access

Peer reviewed

Calcific Aortic Valve Stenosis: Methods, Models, and Mechanisms

Jordan D Miller, Robert M Weiss and Donald D Heistad

Circulation research, Vol.108(11), pp.1392-1412

05/27/2011

DOI: 10.1161/CIRCRESAHA.110.234138

PMCID: PMC3150727

PMID: 21617136

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Abstract

Calcific aortic valve stenosis (CAVS) is a major health problem facing aging societies. The identification of osteoblast-like and osteoclast-like cells in human tissue has led to a major paradigm shift in the field. CAVS was thought to be a passive, degenerative process, whereas now the progression of calcification in CAVS is considered to be actively regulated. Mechanistic studies examining the contributions of true ectopic osteogenesis, non-osseous calcification, and ectopic osteoblast-like cells (that appear to function differently from skeletal osteoblasts) to valvular dysfunction have been facilitated by the development of mouse models of CAVS. Recent studies also suggest that valvular fibrosis, as well as calcification, may play an important role in restricting cusp movement, and CAVS may be more appropriately viewed as a fibrocalcific disease. High resolution echocardiography and magnetic resonance imaging have emerged as useful tools for testing the efficacy of pharmacological and genetic interventions in vivo . Key studies in humans and animals are reviewed that have shaped current paradigms in the field of CAVS, and suggest promising future areas for research.

Animal Models

fibrosis

calcification

phenotyping

echocardiography

Details

Title: Subtitle: Calcific Aortic Valve Stenosis: Methods, Models, and Mechanisms
Creators: Jordan D Miller - Department of Surgery and Physiology, Mayo Clinic
Robert M Weiss - Department of Internal Medicine, University of Iowa Carver College of Medicine
Donald D Heistad - Department of Internal Medicine, University of Iowa Carver College of Medicine
Resource Type: Journal article
Publication Details: Circulation research, Vol.108(11), pp.1392-1412
DOI: 10.1161/CIRCRESAHA.110.234138
PMID: 21617136
PMCID: PMC3150727
NLM abbreviation: Circ Res
ISSN: 0009-7330
eISSN: 1524-4571
Grant note: R00 HL092235-04 || HL / National Heart, Lung, and Blood Institute : NHLBI R00 HL092235-03 || HL / National Heart, Lung, and Blood Institute : NHLBI
Language: English
Date published: 05/27/2011
Academic Unit: Cardiovascular Medicine; Neuroscience and Pharmacology; Internal Medicine
Record Identifier: 9984040373902771

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