Reactive Oxygen-Forming Nox5 Links Vascular Smooth Muscle Cell Phenotypic Switching and Extracellular Vesicle-Mediated Vascular Calcification.

Conclusions: We show here that contractile VSMCs are resistant to calcification and identify Nox5 as a key regulator of VSMC phenotypic switching. Additionally, we describe a new mechanism of Ca2+ uptake via EVs and show that Ca2+ induces ROS production in VSMCs via Nox5. ROS production is required for release of EVs, which promote calcification. Identifying molecular pathways that control Nox5 and VSMC-derived EVs provides potential targets to modulate vascular remodelling and calcification in the context of mineral imbalance.
PMID: 32564697 [PubMed - as supplied by publisher]

Source: Circulation Research - June 21, 2020 Category: Cardiology Authors: Furmanik M, Chatrou M, van Gorp RH, Akbulut A, Willems B, Schmidt HH, van Eys G, Bochaton-Piallat ML, Proudfoot D, Biessen EA, Hedin U, Matic L, Mees B, Shanahan CM, Reutelingsperger C, Schurgers LJ Tags: Circ Res Source Type: research