BMP antagonists enhance myogenic differentiation and ameliorate the dystrophic phenotype in a DMD mouse model

Autor: SongTing Shi, Willem M.H. Hoogaars, David J.J. de Gorter, Sandra H. van Heiningen, Herbert Y. Lin, Charles C. Hong, Dwi U. Kemaladewi, Annemieke Aartsma-Rus, Peter ten Dijke, Peter A.C. 't Hoen

Publikováno v: Neurobiology of Disease, Vol 41, Iss 2, Pp 353-360 (2011)

Duchenne Muscular Dystrophy (DMD) is an X-linked lethal muscle wasting disease characterized by muscle fiber degeneration and necrosis. The progressive pathology of DMD can be explained by an insufficient regenerative response resulting in fibrosis a

Externí odkaz: https://doaj.org/article/e99658d68de6481c933e95f75cc94599

Reduced growth rate of aged muscle stem cells is associated with impaired mechanosensitivity

Autor: Mohammad Haroon, Heleen E. Boers, Astrid D. Bakker, Niek G.C. Bloks, Willem M.H. Hoogaars, Lorenzo Giordani, René J.P. Musters, Louise Deldicque, Katrien Koppo, Fabien Le Grand, Jenneke Klein-Nulend, Richard T. Jaspers

Publikováno v: Aging (Albany NY)
Aging, 14(1), 28-53. Impact Journals
Aging, 14(1), 28-53. US Administration on Aging
Haroon, M, Boers, H E, Bakker, A D, Bloks, N G C, Hoogaars, W M H, Giordani, L, Musters, R J P, Deldicque, L, Koppo, K, Grand, F L, Klein-Nulend, J & Jaspers, R T 2022, ' Reduced growth rate of aged muscle stem cells is associated with impaired mechanosensitivity ', Aging, vol. 14, no. 1, pp. 28-53 . https://doi.org/10.18632/aging.203830
Aging, Vol. 14, no.1, p. 28-53 (2022)
Aging
Aging, In press, 14 (1), pp.28-53. ⟨10.18632/aging.203830⟩

Aging-associated muscle wasting and impaired regeneration are caused by deficiencies in muscle stem cell (MuSC) number and function. We postulated that aged MuSCs are intrinsically impaired in their responsiveness to omnipresent mechanical cues throu

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::83874a44facb58bcc44a752a6d5e2d90
https://pubmed.ncbi.nlm.nih.gov/35023852

TGF-β Regulates Collagen Type I Expression in Myoblasts and Myotubes via Transient Ctgf and Fgf-2 Expression

Autor: Richard T. Jaspers, Michèle M. G. Hillege, Ricardo A. Galli Caro, Carla Offringa, Gerard M.J. de Wit, Willem M.H. Hoogaars

Publikováno v: Hillege, M M G, Galli Caro, R A, Offringa, C, de Wit, G M J, Jaspers, R T & Hoogaars, W M H 2020, ' TGF-β Regulates Collagen Type I Expression in Myoblasts and Myotubes via Transient Ctgf and Fgf-2 Expression ', Cells, vol. 9, no. 2 . https://doi.org/10.3390/cells9020375
Hillege, M M G, Galli Caro, R A, Offringa, C, de Wit, G M J, Jaspers, R T & Hoogaars, W M H 2020, ' TGF-β Regulates Collagen Type I Expression in Myoblasts and Myotubes via Transient Ctgf and Fgf-2 Expression ', Cells, vol. 9, no. 2, 375, pp. 1-21 . https://doi.org/10.3390/cells9020375
Cells, 9(2). MDPI Multidisciplinary Digital Publishing Institute
Cells
Volume 9
Issue 2
Cells, 9(2):375, 1-21. MDPI Multidisciplinary Digital Publishing Institute
Cells, Vol 9, Iss 2, p 375 (2020)

Transforming Growth Factor β (TGF-β) is involved in fibrosis as well as the regulation of muscle mass, and contributes to the progressive pathology of muscle wasting disorders. However, little is known regarding the time-dependent signalling of TGF

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::90c3ec33cd6019607e73478420487df1
https://research.vumc.nl/en/publications/cd94bfbc-2bc8-4bb7-b87c-55f11c00d298

Inhibition of Activin Signaling Slows Progression of Polycystic Kidney Disease

Autor: Fatiha el Bouazzaoui, Emile de Heer, Olli Ritvos, Dorien J.M. Peters, Kimberley Veraar, Sebastian B.T. Jianu, Wouter N. Leonhard, Arja Pasternack, Martijn H. Breuning, Steven J. Kunnen, Peter ten Dijke, Willem M.H. Hoogaars, Anna J. Plugge

Publikováno v: Journal of the American Society of Nephrology, 27(12), 3589-3599
Journal of the American Society of Nephrology, 27(12), 3589-3599. American Society of Nephrology
Journal of the American Society of Nephrology
Leonhard, W M, Kunnen, S J, Plugge, A J, Pasternack, A, Jianu, B, Veraar, K, El Bouazzaoui, F, Hoogaars, W, ten Dijke, P, Breuning, M H, de Heer, E, Ritvos, O & Peters, D J 2016, ' Inhibition of Activin Signaling Slows Progression of Polycystic Kidney Disease. ', Journal of the American Society of Nephrology, vol. 27, no. 12, pp. 3589-3599 . https://doi.org/10.1681/ASN.2015030287

Autosomal dominant polycystic kidney disease (ADPKD), characterized by the formation of numerous kidney cysts, is caused by PKD1 or PKD2 mutations and affects 0.1% of the population. Although recent clinical studies indicate that reduction of cAMP le

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::93782ea39509f693d8ac7032c683b38c
https://research.vu.nl/en/publications/e444f41f-b3bc-433c-aa69-cc88d1c628e4

New function of the myostatin/activin type I receptor (ALK4) as a mediator of muscle atrophy and muscle regeneration

Autor: Ron Wolterbeek, Maurice Overzier, Maaike van Putten, Willem M.H. Hoogaars, Ksenia Lezhnina, Annemieke Aartsma-Rus, Ivan V. Ozerov, Svitlana Pasteuning-Vuhman, Peter ten Dijke, Cindy J.M. Loomans, Aliper Aleksandr M, Joke W. Boertje-van der Meulen, Szymon M. Kielbasa, Wibowo Arindrarto

Publikováno v: Pasteuning-Vuhman, S, Boertje-van der Meulen, J, van Putten, M, Overzier, M, ten Dijke, P, Kiełbasa, S M, Arindrarto, W, Wolterbeek, R, Lezhnina, K V, Ozerov, I V, Aliper, A M, Hoogaars, W, Aartsma-Rus, A & Loomans, C J 2017, ' New function of the myostatin/activin type I receptor (ALK4) as a mediator of muscle atrophy and muscle regeneration. ', FASEB Journal, vol. 31, no. 1, pp. 238-255 . https://doi.org/10.1096/fj.201600675R
The FASEB Journal
FASEB Journal, 31(1), 238-255
FASEB Journal, 31(1), 238-255. FASEB

Skeletal muscle fibrosis and impaired muscle regeneration are major contributors to muscle wasting in Duchenne muscular dystrophy (DMD). Muscle growth is negatively regulated by myostatin (MSTN) and activins. Blockage of these pathways may improve mu

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8d4e61605dd5e02f46831fcc46708d0b
https://hdl.handle.net/1871.1/7b2791f0-8be7-445f-8439-56f930648ed7