March 2021 - Ouafa Hamza

DDr. Ouafa Hamza

MedUni Wien RESEARCHER OF THE MONTH March 2021

Tenascin C promotes valvular remodeling in two large animal models of ischemic mitral regurgitation

Ischemic mitral valve regurgitation is a frequent complication of myocardial infarction. It involves a complex mechano-physiological process combining a LV remodelling, mitral annular dilatation, and valvular tethering. This leads to an impaired mitral leaflet closure and ultimately to the development of mitral regurgitation and subsequently worse clinical outcome. The observations of DDr. Hamza et al. (1) suggest that Tenascin C, an extracellular matrix glycoprotein, plays a role in altering valvular flexibility by enhancing endothelial to mesenchymal transition (EMT), which can be reduced by TLR4 blockade. Better understanding the mechanisms involved in leaflet fibrosis and excess EMT is crucial to modulate the cellular processes and guide them towards increasing leaflet area without compromising their flexibility and their coaptation. These new findings open new therapeutic options for patients with mitral regurgitation.

Selected Literature

1. Tenascin C promotes valvular remodeling in two large animal models of ischemic mitral regurgitation.Hamza O, Kiss A, Kramer AM, Trojanek S, Abraham D, Acar E, Nagel F, Tretter VE, Kitzwögerer M, Podesser BK.Basic Res Cardiol. 2020 Dec 1;115(6):76. doi:10.1007/s00395-020-00837-5.PMID: 33258993
2. Bursi F, Enriquez-Sarano M, Nkomo VT, Jacobsen SJ, Weston SA, Meverden RA, Roger VL (2005) Heart failure and death after myocardial infarction in the community: The emerging role of mitral regurgitation. Circulation 111:295–301.
3. Hamza O, Kiss A, Kramer AM, Tillmann KE, Podesser BK. EuroIntervention. 2020 Aug 7;16(6):e518-e522. doi:10.4244/EIJ-D-19-00095.PMID: 31235459