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Osteogenesis imperfecta (OI) is the most typical genetic type of brittle bone illness and leads to defects of each bone and connective tissue. OI sufferers can have vital issues with mobility as a result of joint dysfunction due partly to tendinopathy. In a brand new examine revealed within the journal Proceedings of the Nationwide Academy of Sciences, researchers at Baylor Faculty of Medication determine a protein signaling mechanism driving this dysfunction and discover that inhibiting this signaling pathway can forestall onset of tendinopathy issues in mouse fashions.
The researchers studied mouse fashions of OI