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Vascular calcification and cellular signaling pathways as potential therapeutic targets.
Kang, Jeong-Hun; Kawano, Takahito; Murata, Masaharu; Toita, Riki.
Afiliação
  • Kang JH; National Cerebral and Cardiovascular Center Research Institute, 6-1 Shinmachi, Kishibe, Suita, Osaka 564-8565, Japan. Electronic address: jrjhkang@ncvc.go.jp.
  • Kawano T; Center for Advanced Medical Innovation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
  • Murata M; Center for Advanced Medical Innovation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan.
  • Toita R; Biomedical Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), 1-8-31 Midorigaoka, Ikeda, Osaka, 563-8577, Japan; AIST-Osaka University Advanced Photonics and Biosensing Open Innovation Laboratory, AIST, 2-1 Yamadaoka, Suita, Osaka 565-0871, Japan.
Life Sci ; 336: 122309, 2024 Jan 01.
Article em En | MEDLINE | ID: mdl-38042282
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.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Aterosclerose / Calcificação Vascular Limite: Humans Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Aterosclerose / Calcificação Vascular Limite: Humans Idioma: En Ano de publicação: 2024 Tipo de documento: Article