Commentary: Aortic valve calcification: A new story with a twist?

Abstract

Schematic of the TWIST1/MATTL3 pathway in osteogenic differentiation of interstitial cells. CENTRAL MESSAGE A novel therapeutic target using the TWIST pathway and valvular interstitial cells may prevent aortic valve calcification.

The Complex Interplay of Inflammation, Metabolism, Epigenetics, and Sex in Calcific Disease of the Aortic Valve

“…It has been reported that changes in RNA/DNA methylation and histone acetylation may have a role in the osteogenic differentiation of VICs. For example it was shown an interesting connection between VICs calcification and N6-methyladenosine (m 6 A) RNA-methylation via the upregulation of methyltransferase-like 3 (METTL3) and repression of the helix-loop-helix transcription factor TWIST ( 82 , 83 ), while in another study, methylation of the NOTCH-1 promoter was found to cause valve calcification through reduction of the NOTCH intracellular domain (NICD) activity and consequent increase of the Wnt/β-Catenin signaling causing enhanced expression of pro-calcific genes. Particularly interesting is the role of NOTCH-1 gene product in valve calcification in an epigenetic perspective.…”

Commentary: Immune cell infiltration in aortic stenosis: Cause or consequence?

“…The importance of preventing calcification cannot be overemphasized, particularly for the longevity of aortic valve repair or reconstruction with or without patch material. 5 , 6 , 7 , 8 , 9 …”

Commentary: From Old World monkeys to New World humans—Evolved protection from tick bites and bioprosthetic material

“… 10 , 11 Less immunogenic materials and improved processing methods have already been described to increase biocompatibility and to prevent an immunologic response to the xenogenic valve tissue. 9 , 11 It appears that a proper understanding of alpha-gal syndrome is important to improve the longevity of bioprosthetic material 13 , 14 , 15 , 16 , 17 in patients with a wide range of congenital and acquired heart disease.…”