Genomes and Genes


Enrique Brandan


Country: Chile


  1. Gonzalez D, Brandan E. CTGF/CCN2 from Skeletal Muscle to Nervous System: Impact on Neurodegenerative Diseases. Mol Neurobiol. 2019;: pubmed publisher
  2. Rebolledo D, Gonzalez D, Faundez Contreras J, Contreras O, Vio C, Murphy Ullrich J, et al. Denervation-induced skeletal muscle fibrosis is mediated by CTGF/CCN2 independently of TGF-β. Matrix Biol. 2019;: pubmed publisher
    ..These results suggest that in our model CTGF/CCN2 is not up-regulated by canonical TGF-β signaling early after denervation and that other factors are likely involved in the early fibrotic response following skeletal muscle denervation. ..
  3. Brandan E. Heparan sulfate provides a mechanism to respond to FGFR2b and control regenerative expansion. J Cell Commun Signal. 2015;9:89 pubmed publisher
    ..This is allowed by the synthesis of 3-O-sulfated heparan sulfate that up-regulate KIT and 3-O-sulfotransferase enzymes, augmenting 3-O-sulfated heparan sulfate. ..
  4. Contreras O, Rebolledo D, Oyarzún J, Olguín H, Brandan E. Connective tissue cells expressing fibro/adipogenic progenitor markers increase under chronic damage: relevance in fibroblast-myofibroblast differentiation and skeletal muscle fibrosis. Cell Tissue Res. 2016;364:647-60 pubmed publisher
  5. request reprint
    Acuña M, Brandan E. Analysis of Pathological Activities of CCN2/CTGF in Muscle Dystrophy. Methods Mol Biol. 2017;1489:513-521 pubmed
    ..We summarize the techniques used to detect CTGF in the skeletal muscle of dystrophic mdx mice. ..
  6. Brandan E, Gutierrez J. Role of skeletal muscle proteoglycans during myogenesis. Matrix Biol. 2013;32:289-97 pubmed publisher
    ..This review is focussed on the advances reached to understand the role of PGs during myogenesis and skeletal muscular dystrophies. ..
  7. Contreras O, Brandan E. Fibro/adipogenic progenitors safeguard themselves: a novel mechanism to reduce fibrosis is discovered. J Cell Commun Signal. 2017;11:77-78 pubmed publisher
    ..Rando's Lab describes that an intronic polyadenylation of Pdgfra regulates FAPs activity, and therefore fibrosis. This discovery opens a new potential target for treating fibrosis. ..
  8. Contreras O, Villarreal M, Brandan E. Nilotinib impairs skeletal myogenesis by increasing myoblast proliferation. Skelet Muscle. 2018;8:5 pubmed publisher
  9. Brandan E, Cabello Verrugio C, Vial C. Novel regulatory mechanisms for the proteoglycans decorin and biglycan during muscle formation and muscular dystrophy. Matrix Biol. 2008;27:700-8 pubmed publisher

More Information


  1. Gutierrez J, Cabrera D, Brandan E. Glypican-1 regulates myoblast response to HGF via Met in a lipid raft-dependent mechanism: effect on migration of skeletal muscle precursor cells. Skelet Muscle. 2014;4:5 pubmed publisher
    ..In addition, glypican-1 was required for in vitro and in vivo HGF-dependent myoblast migration. Glypican-1 is a regulator of HGF-dependent signaling via Met in lipid raft domains. ..
  2. Morales M, Acuña M, Cabrera D, Goldschmeding R, Brandan E. The pro-fibrotic connective tissue growth factor (CTGF/CCN2) correlates with the number of necrotic-regenerative foci in dystrophic muscle. J Cell Commun Signal. 2018;12:413-421 pubmed publisher
    ..Thus, CCN2 appears to be involved in the fibrotic response as well as in the inflammatory response in the dystrophic skeletal muscle. ..
  3. Acuña M, Salas D, Córdova Casanova A, Cruz Soca M, Cespedes C, Vio C, et al. Blockade of Bradykinin receptors worsens the dystrophic phenotype of mdx mice: differential effects for B1 and B2 receptors. J Cell Commun Signal. 2018;12:589-601 pubmed publisher
    ..These results indicate that the endogenous KKS has a protective role in the dystrophic muscle. The KKS may be a new target for future therapies to reduce inflammation and fibrosis in dystrophic muscle. ..