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Investigating Aortic Valve Calcification via Isolation and Culture of T Lymphocytes using Feeder Cells from Irradiated Buffy Coat
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Investigating Aortic Valve Calcification via Isolation and Culture of T Lymphocytes using Feeder Cells from Irradiated Buffy Coat

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Calcific Aortic Valve Disease-Natural History and Future Therapeutic Strategies

Brunilda Alushi1,2, Lavinia Curini1,3, Mary Roxana Christopher1

  • 1Department of Cardiology, Charite´ Universitätsmedizin Berlin and German Centre for Cardiovascular Research (DZHK), Berlin, Germany.

Frontiers in Pharmacology
|June 2, 2020
PubMed

Insights

Calcific aortic valve disease (CAVD) involves inflammation and mineralization, leading to heart valve narrowing. Understanding the roles of epigenetics and the microbiome may reveal new therapeutic strategies for this common heart disorder.

Area of Science:

  • Cardiovascular Medicine
  • Pathophysiology
  • Molecular Biology

Background:

  • Calcific aortic valve disease (CAVD) is the most common heart valve disorder, characterized by valve mineralization and impaired blood flow.
  • Its pathophysiology is complex, involving genetic, inflammatory, and lipid-related factors, but the progression from inflammation to stenosis is not fully understood.
  • Current research limitations include a lack of longitudinal studies due to the unavailability of early-stage CAVD samples.

Purpose of the Study:

  • To review the current understanding of CAVD pathophysiology.
  • To discuss emerging roles of non-coding RNAs and the microbiome in CAVD.
  • To explore potential future therapeutic strategies for CAVD.

Main Methods:

  • Literature review and synthesis of existing research on CAVD.
  • Analysis of the interplay between inflammation, calcification, epigenetics, and the microbiome in CAVD.
  • Discussion of current and potential future therapeutic interventions.

Main Results:

  • CAVD involves active remodeling, mineralization, and inflammation, leading to aortic valve stenosis.
  • Epigenetic markers, including non-coding RNAs, are increasingly implicated in CAVD's phenotypic changes.
  • The microbiome is emerging as a potential contributor to the inflammatory processes in CAVD.

Conclusions:

  • The precise pathways from inflammation to calcification and stenosis in CAVD require further elucidation.
  • Epigenetic factors and the microbiome represent promising avenues for understanding CAVD pathogenesis.
  • Targeting inflammation, calcification, epigenetics, and the microbiome may offer novel therapeutic strategies for CAVD.

Keywords:
TAVRaortic valve replacementcalcific aortic valveimmune systeminflammationmicrobiomesevere aortic stenosis

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