The Dualistic Role of Macrophages in Aortic Valve Calcification
Résumé
Calcific aortic valve stenosis (CAS) is the most common
valvular heart disease worldwide, associated with cardiovascular
morbidity and mortality. This pathology results from fibro-
calcific degeneration of the aortic valve leaflets, causing major
cardiovascular complications. To date, drug therapies have been
ineffective in preventing the progression of CAS and aortic valve
replacement remains the mainstay of management for patients
with symptomatic CAS. Unfortunately, not all patients are
eligible for this procedure, which is associated with a greater risk
of mortality for subjects presenting comorbidities. A better
understanding of the mechanisms responsible for CAS
pathogenesis is therefore of crucial importance to develop new
therapeutic strategies. Inflammation is a key driver of aortic
valve fibrosis and calcification. Macrophages, which play critical
roles in the induction and resolution of sterile inflammation, may
therefore represent interesting therapeutic targets. Once
infiltrated within the aortic leaflet, these dynamic cells can adopt
a pro-inflammatory M1 phenotype or switch toward an
alternatively activated M2 phenotype, resulting in wound healing
and anti-inflammatory activities. This plasticity complicates the
efforts to understand their role in the initiation and progression
of CAS. This book chapter aims to summarize our current
knowledge regarding the role played by macrophage subsets on
aortic valve remodelling.
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