[CKD-MBD (Chronic Kidney Disease-Mineral and Bone Disorder). Gene therapy for secondary hyperparathyroidism].
Secondary hyperparathyroidism (SHPT) is one of the most important complications of chronic kidney disease. Although 1,25-D pulse therapy is effective for SHPT, hyperplastic parathyroid (PT) cells gradually develop resistance to 1,25-D. Vitamin D(3) receptor (VDR) levels are decreased in the PT glands of dialysis patients and animal models of renal failure. To develop a new approach to such rebellious tissue, recent research has shown that the functionality protein can be adjusted with the gene transfer to the parathyroid. The experiment using adenovirus clarifies that the gene transfer of VDR and calcium sensing receptor is enabled, and such a gene expression is induced. In the recent research, we examined both in vitro and in vivo the potential use of RNAi to suppress PTH production in PT cells of SHPT patients. These results provide the findings to understand the mechanism and new treatment to SHPT.
Kanai
Genta
G
Division of Nephrology and Metabolism, Tokai University School of Medicine.
Fukagawa
Masafumi
M
D000256:Adenoviridae; D001851:Bone Diseases, Metabolic / Q000209:etiology*; D002908:Chronic Disease; D016503:Drug Delivery Systems; D015316:Genetic Therapy; D005822:Genetic Vectors; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000209:etiology* / Q000628:therapy*; D006965:Hyperplasia; D007674:Kidney Diseases / Q000150:complications*; D010280:Parathyroid Glands / Q000166:cytology / Q000378:metabolism / Q000473:pathology; D010281:Parathyroid Hormone / Q000378:metabolism; D034622:RNA Interference; D034741:RNA, Small Interfering / Q000008:administration & dosage; D018167:Receptors, Calcitriol / Q000235:genetics; D044169:Receptors, Calcium-Sensing / Q000235:genetics
D010281:Parathyroid Hormone; D034741:RNA, Small Interfering; D018167:Receptors, Calcitriol; D044169:Receptors, Calcium-Sensing