TY - JOUR
T1 - Vascular calcification and cellular signaling pathways as potential therapeutic targets
AU - Kang, Jeong Hun
AU - Kawano, Takahito
AU - Murata, Masaharu
AU - Toita, Riki
N1 - Publisher Copyright:
© 2023
PY - 2024/1/1
Y1 - 2024/1/1
N2 - Increased vascular calcification (VC) is observed in patients with cardiovascular diseases such as atherosclerosis, diabetes, and chronic kidney disease. VC is divided into three types according to its location: intimal, medial, and valvular. Various cellular signaling pathways are associated with VC, including the Wnt, mitogen-activated protein kinase, phosphatidylinositol-3 kinase/Akt, cyclic nucleotide-dependent protein kinase, protein kinase C, calcium/calmodulin-dependent kinase II, adenosine monophosphate-activated protein kinase/mammalian target of rapamycin, Ras homologous GTPase, apoptosis, Notch, and cytokine signaling pathways. In this review, we discuss the literature concerning the key cellular signaling pathways associated with VC and their role as potential therapeutic targets. Inhibitors to these pathways represent good candidates for use as potential therapeutic agents for the prevention and treatment of VC.
AB - Increased vascular calcification (VC) is observed in patients with cardiovascular diseases such as atherosclerosis, diabetes, and chronic kidney disease. VC is divided into three types according to its location: intimal, medial, and valvular. Various cellular signaling pathways are associated with VC, including the Wnt, mitogen-activated protein kinase, phosphatidylinositol-3 kinase/Akt, cyclic nucleotide-dependent protein kinase, protein kinase C, calcium/calmodulin-dependent kinase II, adenosine monophosphate-activated protein kinase/mammalian target of rapamycin, Ras homologous GTPase, apoptosis, Notch, and cytokine signaling pathways. In this review, we discuss the literature concerning the key cellular signaling pathways associated with VC and their role as potential therapeutic targets. Inhibitors to these pathways represent good candidates for use as potential therapeutic agents for the prevention and treatment of VC.
KW - Cardiovascular disease
KW - Heart
KW - Inhibitor
KW - Mineralization
KW - Signaling pathway
KW - Vessel
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U2 - 10.1016/j.lfs.2023.122309
DO - 10.1016/j.lfs.2023.122309
M3 - Review article
C2 - 38042282
AN - SCOPUS:85179059592
SN - 0024-3205
VL - 336
JO - Life Sciences
JF - Life Sciences
M1 - 122309
ER -
