Inflammatory and Biomechanical Drivers of Endothelial-Interstitial Interactions in Calcific Aortic Valve Disease

Circ Res. 2021 Apr 30;128(9):1344-1370. doi: 10.1161/CIRCRESAHA.121.318011. Epub 2021 Apr 29.

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