Type I Angiotensin II Receptor Blockade Reduces Uremia-Induced Deterioration of Bone Material Properties
| Autor: | Junichiro James Kazama, Masafumi Fukagawa, Ryosuke Ozasa, Takayoshi Nakano, Shingo Fukuma, Suguru Yamamoto, Akemi Ito, Shin Goto, Shunichi Fukuhara, Yoshihiro Onishi, Takuya Wakamatsu, Koji Matsuo, Hideyuki Yamato, Chisato Miyakoshi, Tadao Akizawa, Ichiei Narita, Yoshiko Iwasaki, Kennichi Tanaka |
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| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
medicine.medical_specialty Angiotensin receptor Endocrinology Diabetes and Metabolism 030209 endocrinology & metabolism medicine.disease_cause Bone and Bones 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Bone Density Internal medicine Renin–angiotensin system medicine Animals Humans Orthopedics and Sports Medicine Renal Insufficiency Chronic Pentosidine Uremia Receptors Angiotensin business.industry medicine.disease Rats 030104 developmental biology Endocrinology medicine.anatomical_structure chemistry Osteocyte Olmesartan business Oxidative stress medicine.drug Kidney disease |
| Zdroj: | Journal of Bone and Mineral Research. 36(1):67-79 |
| ISSN: | 1523-4681 |
| Popis: | Wakamatsu T., Iwasaki Y., Yamamoto S., et al. Type I Angiotensin II Receptor Blockade Reduces Uremia-Induced Deterioration of Bone Material Properties. Journal of Bone and Mineral Research, 36, 1, 67. https://doi.org/10.1002/jbmr.4159. Chronic kidney disease (CKD) is associated with a high incidence of fractures. However, the pathophysiology of this disease is not fully understood, and limited therapeutic interventions are available. This study aimed to determine the impact of type 1 angiotensin II receptor blockade (AT-1RB) on preventing CKD-related fragility fractures and elucidate its pharmacological mechanisms. AT-1RB use was associated with a lower risk of hospitalization due to fractures in 3276 patients undergoing maintenance hemodialysis. In nephrectomized rats, administration of olmesartan suppressed osteocyte apoptosis, skeletal pentosidine accumulation, and apatite disorientation, and partially inhibited the progression of the bone elastic mechanical properties, while the bone mass was unchanged. Olmesartan suppressed angiotensin II-dependent oxidation stress and apoptosis in primary cultured osteocytes in vitro. In conclusion, angiotensin II-dependent intraskeletal oxidation stress deteriorated the bone elastic mechanical properties by promoting osteocyte apoptosis and pentosidine accumulation. Thus, AT-1RB contributes to the underlying pathogenesis of abnormal bone quality in the setting of CKD, possibly by oxidative stress. © 2020 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR). |
| Databáze: | OpenAIRE |
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