MedElevator Войти в исследования
← Поиск публикаций

DOI 10.1038/nrendo.2016.12

Медицинская библиотека · Nature reviews. Endocrinology · 2016

BMP signalling in skeletal development, disease and repair.

Salazar Valerie S, Gamer Laura W, Rosen Vicki

СтатьяОбзорПеревод в очереди

Аннотация

Since the identification in 1988 of bone morphogenetic protein 2 (BMP2) as a potent inducer of bone and cartilage formation, BMP superfamily signalling has become one of the most heavily investigated topics in vertebrate skeletal biology. Whereas a large part of this research has focused on the roles of BMP2, BMP4 and BMP7 in the formation and repair of endochondral bone, a large number of BMP superfamily molecules have now been implicated in almost all aspects of bone, cartilage and joint biology. As modulating BMP signalling is currently a major therapeutic target, our rapidly expanding knowledge of how BMP superfamily signalling affects most tissue types of the skeletal system creates enormous potential to translate basic research findings into successful clinical therapies that improve bone mass or quality, ameliorate diseases of skeletal overgrowth, and repair damage to bone and joints. This Review examines the genetic evidence implicating BMP superfamily signalling in vertebrate bone and joint development, discusses a selection of human skeletal disorders associated with altered BMP signalling and summarizes the status of modulating the BMP pathway as a therapeutic target for skeletal trauma and disease.

Для цитирования: Salazar Valerie S, Gamer Laura W, Rosen Vicki. BMP signalling in skeletal development, disease and repair.. Nature reviews. Endocrinology. 2016. DOI: 10.1038/nrendo.2016.12.

Предметные рубрики MeSH

Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…

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.

Тип публикации указан по данным источника. Уровень доказательности автоматически не присваивается.