In 1987, Robert Davis, Hal Weintraub and I reported the identification of MyoD, a transcription factor that could reprogram fibroblasts into skeletal muscle cells. In this recollection, I both summarize the prior work of Helen Blau, Woody Wright, Peter Jones and Charlie Emerson that inspired my entry into this field, and the subsequent events that led to finding MyoD. Lastly, I highlight some of the principles in developmental biology that have emerged during the past 30 years, which are particularly relevant to skeletal muscle biology.
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http://dx.doi.org/10.1016/j.semcdb.2017.10.021 | DOI Listing |
Lasers Med Sci
January 2025
Department of Bioscience, Federal University of São Paulo, R. Silva Jardim, 136, Vila Mathias, Santos, Sao Paulo, 11015-020, Brazil.
The aim of this study was to evaluate the effectiveness of an aquatic progressive resistance exercise (APRE) and PBM (associated or not) on morphology of skeletal muscle and biochemical markers using an experimental model of knee osteoarthritis (OA). Fifty male Wistar rats were randomly distributed into 5 groups: control group (CG); OA control (OAC); OA submitted to APRE (OAE); OA submitted to PBM (OAL); OA submitted to APRE and PBM (OAEL). Trained rats performed a water-jumping program carrying a load equivalent to 50-80% of their body mass strapped to their chest.
View Article and Find Full Text PDFCells
January 2025
Department of Biochemistry, Dongguk University College of Medicine, 123 Dongdae-ro, Gyeongju 38066, Republic of Korea.
An actin-binding protein, known as Calponin 3 (CNN3), modulates the remodeling of the actin cytoskeleton, a fundamental process for the maintenance of skeletal muscle homeostasis. Although the roles of CNN3 in actin remodeling have been established, its biological significance in myoblast differentiation remains largely unknown. This study investigated the functional significance of CNN3 in myogenic differentiation, along with its effects on actin remodeling and mechanosensitive signaling in C2C12 myoblasts.
View Article and Find Full Text PDFSkelet Muscle
January 2025
Department of Anesthesia and Critical Care, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Background: Duchenne muscular dystrophy (DMD) is a prevalent, fatal degenerative muscle disease with no effective treatments. Mdx mouse model of DMD exhibits impaired muscle performance, oxidative stress, and dysfunctional autophagy. Although antioxidant treatments may improve the mdx phenotype, the precise molecular mechanisms remain unclear.
View Article and Find Full Text PDFZhonghua Bing Li Xue Za Zhi
January 2025
Department of Pathology, West China Hospital, Sichuan University, Chengdu610041, China.
Stem Cells Int
December 2024
Shanghai Key Laboratory of Craniomaxillofacial Development and Diseases, Shanghai Stomatological Hospital and School of Stomatology, Fudan University, Shanghai, China.
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