Bone reports · 2026
Irisin fails to rescue bone loss in a rat model of chronic kidney disease - mineral bone disorder (CKD-MBD) but interacts with parathyroid hormone (PTH) in vivo and in vitro in IDG-SW3 osteocytes.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wilson Hannah E, Chen Neal X, O'Neill Kalisha D, Metzger Corinne E, Srinivasan Shruthi, Stephen Daniel J, Blacklock Karis, Matter Emily K, Bonewald Lynda F, Allen Matthew R, Moe Sharon M
Аннотация
INTRODUCTION: Chronic kidney disease progression leads to bone loss and increased fracture and mortality risk. The myokine irisin, produced by muscle during exercise, has been shown to exert protective effects on bone in healthy animals and exhibits a potential interaction with PTH in vitro. The aims of this study were to determine the effect of irisin on bone in CKD-MBD and determine if an interaction exists with PTH in vitro and in vivo.
METHODS: Early and mature IDG-SW3 osteocytes were treated with recombinant irisin, PTH, or both. Mineralization and osteocyte cell markers were assessed. In a similar 2 × 2 design, male Cy/+IU (CKD-MBD) rats were treated with or without irisin under high and low PTH conditions. Dynamic histomorphometry, bone structure, mechanical properties, and musculoskeletal gene markers were assessed.
RESULTS: In vitro, irisin alone downregulated Dkk1 and Sost, inhibitors of bone formation, and PTH receptor mRNA expression, primarily in early osteocytes. However, in the presence of PTH, no effects of irisin were observed. In vivo, the administration of irisin to animals with progressive CKD also downregulated PTH receptor 1 expression but did not affect bone turnover or structure or mechanical properties.
CONCLUSIONS: Irisin did not meaningfully ameliorate bone loss in an animal model of CKD-MBD but did interact with PTH by downregulating its receptor in vitro in osteocytes and in vivo in bone.
METHODS: Early and mature IDG-SW3 osteocytes were treated with recombinant irisin, PTH, or both. Mineralization and osteocyte cell markers were assessed. In a similar 2 × 2 design, male Cy/+IU (CKD-MBD) rats were treated with or without irisin under high and low PTH conditions. Dynamic histomorphometry, bone structure, mechanical properties, and musculoskeletal gene markers were assessed.
RESULTS: In vitro, irisin alone downregulated Dkk1 and Sost, inhibitors of bone formation, and PTH receptor mRNA expression, primarily in early osteocytes. However, in the presence of PTH, no effects of irisin were observed. In vivo, the administration of irisin to animals with progressive CKD also downregulated PTH receptor 1 expression but did not affect bone turnover or structure or mechanical properties.
CONCLUSIONS: Irisin did not meaningfully ameliorate bone loss in an animal model of CKD-MBD but did interact with PTH by downregulating its receptor in vitro in osteocytes and in vivo in bone.