Abstract
Calcific aortic valve disease is dramatically increasing in global burden, yet no therapy exists outside of prosthetic replacement. The increasing proportion of younger and more active patients mandates alternative therapies. Studies suggest a window of opportunity for biologically based diagnostics and therapeutics to alleviate or delay calcific aortic valve disease progression. Advancement, however, has been hampered by limited understanding of the complex mechanisms driving calcific aortic valve disease initiation and progression towards clinically relevant interventions.
Keywords:
aortic valve; cardiovascular disease; cytokines; endothelial cells; inflammation.
Publication types
-
Research Support, N.I.H., Extramural
-
Review
MeSH terms
-
Aortic Valve / cytology*
-
Aortic Valve / immunology
-
Aortic Valve / pathology*
-
Aortic Valve / physiology
-
Aortic Valve Stenosis / diagnosis
-
Aortic Valve Stenosis / etiology*
-
Aortic Valve Stenosis / immunology
-
Aortic Valve Stenosis / therapy
-
Calcinosis / diagnosis
-
Calcinosis / etiology*
-
Calcinosis / immunology
-
Calcinosis / therapy
-
Cell Adhesion Molecules / metabolism
-
Disease Progression*
-
Endothelial Cells / physiology*
-
Homeostasis
-
Humans
-
Immune System / physiology
-
Inflammation Mediators / metabolism
-
Nitric Oxide / biosynthesis
-
Nitric Oxide Synthase Type III / metabolism
-
Prognosis
-
Reactive Oxygen Species
-
Risk Factors
-
Vasculitis / etiology
Substances
-
Cell Adhesion Molecules
-
Inflammation Mediators
-
Reactive Oxygen Species
-
Nitric Oxide
-
NOS3 protein, human
-
Nitric Oxide Synthase Type III
Supplementary concepts
-
Aortic Valve, Calcification of