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. 2022 Mar 9;9:783543. doi: 10.3389/fcvm.2022.783543

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Copyright © 2022 Dayawansa, Baratchi and Peter.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Feedback mechanisms that perpetuate valvular inflammation in CAVD. Understanding the drivers of chronic valvular inflammation are key to arresting the progression of CAVD. Following the initiation of valvular inflammation and stenosis, mechanosensitive feedback pathways may provide the coupling link that promotes further VIC differentiation and valvular inflammation (TNF-α, tumour necrosis factor alpha; IL-1β, interleukin 1-beta; IL-6, interleukin 6; BMP, bone morphogenetic protein; VIC, valvular interstitial cell; End-MT, endothelial-mesenchymal transition; ECM, extracellular matrix; ROCK, rho-associated protein kinase).