Dysregulated RANK Ligand/RANK Axis in Hyperhomocysteinemic Subjects | Zendy

Marit S. Nenseter | Zendy; Thor Ueland | Zendy; Kjetil Retterstøl | Zendy; Ellen Strøm | Zendy; Lars Mørkrid | Zendy; Sverre Landaas | Zendy; Leiv Ose | Zendy; Pål Aukrust | Zendy; Kirsten B. Holven | Zendy

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Dysregulated RANK Ligand/RANK Axis in Hyperhomocysteinemic Subjects

Author(s) -

Marit S. Nenseter,

Thor Ueland,

Kjetil Retterstøl,

Ellen Strøm,

Lars Mørkrid,

Sverre Landaas,

Leiv Ose,

Pål Aukrust,

Kirsten B. Holven

Publication year - 2008

Publication title -

stroke

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.397

H-Index - 319

eISSN - 1524-4628

pISSN - 0039-2499

DOI - 10.1161/strokeaha.108.522995

Subject(s) - rankl , medicine , peripheral blood mononuclear cell , rank ligand , vitamin d and neurology , osteoprotegerin , endocrinology , hyperhomocysteinemia , inflammation , homocysteine , immunology , receptor , in vitro , biology , activator (genetics) , biochemistry

Homocysteine has been linked to increased risk of ischemic stroke and other cardiovascular events. Matrix degradation and inflammation play an important role in these disorders, and we have demonstrated increased levels of matrix-degrading enzymes and inflammatory cytokines in hyperhomocysteinemic individuals. Recent studies suggest that RANK ligand (RANKL) through interaction with its receptor RANK can modulate matrix degradation and inflammation. The present study aimed to examine the role of the RANKL/RANK axis in hyperhomocystinemia.

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