Angiotensin-converting enzyme inhibitor prevents skeletal muscle fibrosis in diabetic mice.

New findings What is the central question of this study? We questioned whether an angiotensin-converting enzyme (ACE) inhibitor prevents skeletal muscle fibrosis in diabetic mice. What is the main finding and its importance? ACE inhibitor administration prevents the increase in skeletal muscle fibrosis during the early phase after diabetes by streptozotocin. Our findings may provide a new therapeutic target to skeletal muscle abnormalities in diabetes. Abstract Fibrosis is characterized by the excessive production and accumulation of extracellular matrix (ECM) components, including collagen. Although the ECM is an essential component of skeletal muscle, fibrosis may have negative effects on muscle function. On the other hand, skeletal muscle fibrosis was shown to be increased in spontaneous hypertensive rats or and to be prevented by an angiotensin-converting enzyme (ACE) inhibitor, an antihypertensive drug, in dystrophic or myocardial infarction mice. In this study, we therefore analyzed whether 1) increased skeletal muscle fibrosis in streptozotocin (STZ)-induced diabetic mice, and 2) a preventive effect on skeletal muscle fibrosis by administration by an ACE inhibitor. Skeletal muscle fibrosis was significantly increased in STZ-induced diabetic mice compared with control mice from 2 to 14 days post-STZ. ACE inhibitor prevented both skeletal muscle fibrosis and muscle function in STZ mice. Our study demonstrated that ACE inhibitor administration prevents the increase in skeletal muscle fibrosis during the early phase after diabetes. Our findings may provide a new therapeutic target to skeletal muscle abnormalities in diabetes. Future studies are required to clarify whether skeletal muscle fibrosis is also directly linked to physical activity. This article is protected by copyright. All rights reserved.