Jack van Horssen

Summary

Affiliation: VU University Medical Center
Country: The Netherlands

Publications

  1. Nijland P, Witte M, Van het Hof B, van der Pol S, Bauer J, Lassmann H, et al. Astroglial PGC-1alpha increases mitochondrial antioxidant capacity and suppresses inflammation: implications for multiple sclerosis. Acta Neuropathol Commun. 2014;2:170 pubmed publisher
    ..Activation of PGC-1α therefore represents a promising therapeutic strategy to improve mitochondrial function and repress inflammation. ..
  2. request reprint
    van Horssen J, Vos C, Admiraal L, Van Haastert E, Montagne L, van der Valk P, et al. Matrix metalloproteinase-19 is highly expressed in active multiple sclerosis lesions. Neuropathol Appl Neurobiol. 2006;32:585-93 pubmed
    ....
  3. van Horssen J, Schreibelt G, Drexhage J, Hazes T, Dijkstra C, van der Valk P, et al. Severe oxidative damage in multiple sclerosis lesions coincides with enhanced antioxidant enzyme expression. Free Radic Biol Med. 2008;45:1729-37 pubmed publisher
    ..Enhanced antioxidant enzyme production in inflammatory MS lesions may reflect an adaptive defense mechanism to reduce ROS-induced cellular damage. ..
  4. van Horssen J, Drexhage J, Flor T, Gerritsen W, van der Valk P, de Vries H. Nrf2 and DJ1 are consistently upregulated in inflammatory multiple sclerosis lesions. Free Radic Biol Med. 2010;49:1283-9 pubmed publisher
    ....
  5. van Horssen J, Witte M, Ciccarelli O. The role of mitochondria in axonal degeneration and tissue repair in MS. Mult Scler. 2012;18:1058-67 pubmed publisher
    ..Finally, we will briefly review therapeutic strategies aimed at improving mitochondrial metabolism and function under neuroinflammatory conditions...
  6. van Horssen J, van Schaik P, Witte M. Inflammation and mitochondrial dysfunction: A vicious circle in neurodegenerative disorders?. Neurosci Lett. 2017;: pubmed publisher
    ..Here we provide a comprehensive overview on how inflammatory mediators impair mitochondrial metabolism and discuss how defective mitochondria can elicit and potentiate an inflammatory response. ..

Detail Information

Publications6

  1. Nijland P, Witte M, Van het Hof B, van der Pol S, Bauer J, Lassmann H, et al. Astroglial PGC-1alpha increases mitochondrial antioxidant capacity and suppresses inflammation: implications for multiple sclerosis. Acta Neuropathol Commun. 2014;2:170 pubmed publisher
    ..Activation of PGC-1α therefore represents a promising therapeutic strategy to improve mitochondrial function and repress inflammation. ..
  2. request reprint
    van Horssen J, Vos C, Admiraal L, Van Haastert E, Montagne L, van der Valk P, et al. Matrix metalloproteinase-19 is highly expressed in active multiple sclerosis lesions. Neuropathol Appl Neurobiol. 2006;32:585-93 pubmed
    ....
  3. van Horssen J, Schreibelt G, Drexhage J, Hazes T, Dijkstra C, van der Valk P, et al. Severe oxidative damage in multiple sclerosis lesions coincides with enhanced antioxidant enzyme expression. Free Radic Biol Med. 2008;45:1729-37 pubmed publisher
    ..Enhanced antioxidant enzyme production in inflammatory MS lesions may reflect an adaptive defense mechanism to reduce ROS-induced cellular damage. ..
  4. van Horssen J, Drexhage J, Flor T, Gerritsen W, van der Valk P, de Vries H. Nrf2 and DJ1 are consistently upregulated in inflammatory multiple sclerosis lesions. Free Radic Biol Med. 2010;49:1283-9 pubmed publisher
    ....
  5. van Horssen J, Witte M, Ciccarelli O. The role of mitochondria in axonal degeneration and tissue repair in MS. Mult Scler. 2012;18:1058-67 pubmed publisher
    ..Finally, we will briefly review therapeutic strategies aimed at improving mitochondrial metabolism and function under neuroinflammatory conditions...
  6. van Horssen J, van Schaik P, Witte M. Inflammation and mitochondrial dysfunction: A vicious circle in neurodegenerative disorders?. Neurosci Lett. 2017;: pubmed publisher
    ..Here we provide a comprehensive overview on how inflammatory mediators impair mitochondrial metabolism and discuss how defective mitochondria can elicit and potentiate an inflammatory response. ..