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Innate immune cells in the pathophysiology of calcific aortic valve disease: lessons to be learned from atherosclerotic cardiovascular disease?
- Source :
- Basic Research in Cardiology, 117, 1, Basic Research in Cardiology, 117
- Publication Year :
- 2022
-
Abstract
- Contains fulltext : 251910.pdf (Publisher’s version ) (Open Access) Calcific aortic valve disease (CAVD) is the most common valvular disease in the developed world with currently no effective pharmacological treatment available. CAVD results from a complex, multifactorial process, in which valvular inflammation and fibro-calcific remodelling lead to valve thickening and cardiac outflow obstruction. The exact underlying pathophysiology of CAVD is still not fully understood, yet the development of CAVD shows many similarities with the pathophysiology of atherosclerotic cardiovascular disease (ASCVD), such as coronary artery disease. Innate immune cells play a crucial role in ASCVD and might also play a pivotal role in the development of CAVD. This review summarizes the current knowledge on the role of innate immune cells, both in the circulation and in the aortic valve, in the development of CAVD and the similarities and differences with ASCVD. Trained immunity and clonal haematopoiesis of indeterminate potential are proposed as novel immunological mechanisms that possibly contribute to the pathophysiology of CAVD and new possible treatment targets are discussed.
- Subjects :
- Physiology
Cardiovascular Diseases
Physiology (medical)
Aortic Valve
Vascular damage Radboud Institute for Health Sciences [Radboudumc 16]
lnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]
Vascular damage Radboud Institute for Molecular Life Sciences [Radboudumc 16]
Calcinosis
Humans
Aortic Valve Stenosis
Cardiology and Cardiovascular Medicine
Atherosclerosis
Immunity, Innate
Subjects
Details
- ISSN :
- 03008428
- Volume :
- 117
- Database :
- OpenAIRE
- Journal :
- Basic Research in Cardiology
- Accession number :
- edsair.doi.dedup.....a1c225b89cdaa5d4b7428ecc40741455
- Full Text :
- https://doi.org/10.1007/s00395-022-00935-6