TY - JOUR
T1 - Vascular Smooth Muscle Cell Neutral Sphingomyelinase 2 in the Release of Exosomes and Vascular Calcification
AU - Pavlic, Angelina
AU - Bahram Sangani, Nasim
AU - Kerins, Johanna
AU - Nicolaes, Gerry
AU - Schurgers, Leon
AU - Reutelingsperger, Chris
N1 - Funding Information:
A.P., G.N., L.S. and C.R. received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Sklodowska—Curie grant agreement No. 675111 for the project EVOluTION. N.B.S. received funding from Stichting Terre—the Dutch Rett Syndrome Foundation.
Publisher Copyright:
© 2022 by the authors.
PY - 2022/8/16
Y1 - 2022/8/16
N2 - Vascular calcification (VC) is the pathological precipitation of calcium salts in the walls of blood vessels. It is a risk factor for cardiovascular events and their associated mortality. VC can be observed in a variety of cardiovascular diseases and is most prominent in diseases that are associated with dysregulated mineral homeostasis such as in chronic kidney disease. Local factors and mechanisms underlying VC are still incompletely understood, but it is appreciated that VC is a multifactorial process in which vascular smooth muscle cells (VSMCs) play an important role. VSMCs participate in VC by releasing extracellular vesicles (EVs), the extent, composition, and propensity to calcify of which depend on VSMC phenotype and microenvironment. Currently, no targeted therapy is available to treat VC. In-depth knowledge of molecular players of EV release and the understanding of their mechanisms constitute a vital foundation for the design of pharmacological treatments to combat VC effectively. This review highlights our current knowledge of VSMCs in VC and focuses on the biogenesis of exosomes and the role of the neutral Sphingomyelinase 2 (nSMase2).
AB - Vascular calcification (VC) is the pathological precipitation of calcium salts in the walls of blood vessels. It is a risk factor for cardiovascular events and their associated mortality. VC can be observed in a variety of cardiovascular diseases and is most prominent in diseases that are associated with dysregulated mineral homeostasis such as in chronic kidney disease. Local factors and mechanisms underlying VC are still incompletely understood, but it is appreciated that VC is a multifactorial process in which vascular smooth muscle cells (VSMCs) play an important role. VSMCs participate in VC by releasing extracellular vesicles (EVs), the extent, composition, and propensity to calcify of which depend on VSMC phenotype and microenvironment. Currently, no targeted therapy is available to treat VC. In-depth knowledge of molecular players of EV release and the understanding of their mechanisms constitute a vital foundation for the design of pharmacological treatments to combat VC effectively. This review highlights our current knowledge of VSMCs in VC and focuses on the biogenesis of exosomes and the role of the neutral Sphingomyelinase 2 (nSMase2).
KW - Exosomes/pathology
KW - Humans
KW - Muscle, Smooth, Vascular/pathology
KW - Myocytes, Smooth Muscle/pathology
KW - Sphingomyelin Phosphodiesterase
KW - Vascular Calcification/genetics
U2 - 10.3390/ijms23169178
DO - 10.3390/ijms23169178
M3 - (Systematic) Review article
C2 - 36012444
SN - 1661-6596
VL - 23
JO - International journal of molecular sciences
JF - International journal of molecular sciences
IS - 16
M1 - 9178
ER -