Key result
Innate and adaptive immunity drive fibrocalcific remodelling in calcific aortic valve disease via NF-κB pathways.
Understanding the immune mechanisms underlying CAVD highlights potential novel therapeutic targets, such as anti-inflammatory agents, to prevent disease progression.
May inform immunomodulatory trials in CAVD; leaves open whether NF-κB or cytokine inhibition alters clinical progression.
Calcific aortic valve disease (CAVD) is the most common heart valve disorder. CAVD is a chronic process characterized by a pathologic mineralization of valve leaflets. Ectopic mineralization of the aortic valve involves complex relationships with immunity. Studies have highlighted that both innate and adaptive immunity play a role in the development of CAVD. In this regard, accumulating evidence indicates that fibrocalcific remodelling of the aortic valve is associated with activation of the NF-κB pathway. The expression of TNF-α and IL-6 is increased in human mineralized aortic valves and promotes an osteogenic program as well as the mineralization of valve interstitial cells (VICs), the main cellular component of the aortic valve. Different factors, including oxidized lipid species, activate the innate immune response through the Toll-like receptors. Moreover, VICs express 5-lipoxygenase and therefore produce leukotrienes, which may amplify the inflammatory response in the aortic valve. More recently, studies have emphasized that an adaptive immune response is triggered during CAVD. Herein, we are reviewing the link between the immune response and the development of CAVD and we have tried, whenever possible, to keep a translational approach.
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Mathieu et al. (2015) conducted a review in Calcific aortic valve disease (CAVD). Innate and adaptive immunity was evaluated. Both innate and adaptive immunity, driven by factors such as oxidized lipids and the NF-κB pathway, play a crucial role in the fibrocalcific remodelling and development of calcific aortic valve disease.
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