title: Designing drugs that encourage spinal cord injury healing.
abstract: BACKGROUND
  Spinal cord injury (SCI) occurs within seconds, but host responses may take years. Although life expectancy has increased, half of the survivors end up as paraplegics, with many indeed as quadriplegics. Host responses may have multiple effects ranging from inhibiting inflammation to preventing repair and regeneration. Efforts seek to translate exciting results from unsatisfactory animal models to humans.
  
  
  METHODS
  The author reviews the current basic and translational research for SCI treatment that: i) limits secondary injury; and ii) enhances endogenous repair and regeneration. The article provides an emphasis on pro-inflammatory factors (TNF-α, high-mobility group B protein 1) that are targeted to encourage healing.
  
  
  CONCLUSIONS
  Research in the coming years needs to be directed at therapeutic agents - whether drugs, biologics or biomaterials - that encourage repair and regeneration and, at the same time, limit cell death and axonal lesions. The author believes that the process of harnessing the power of these innate responses will remain the challenge for the future in the quest for effective therapeutic options.
authors: University of Kansas Medical Center, Departments of Neurology, Physiology and Pharmacology , Kansas City, KS 66170 , USA.
authors: Barry W
authors: BW
authors: Festoff
mesh_terms: D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects; D002986:Clinical Trials as Topic; D015195:Drug Design; D004353:Drug Evaluation, Preclinical; D024243:HMGB1 Protein / Q000378:metabolism; D006801:Humans; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use*; D013119:Spinal Cord Injuries / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D014945:Wound Healing / Q000187:drug effects*
chemical_list: D000893:Anti-Inflammatory Agents; D024243:HMGB1 Protein; D018696:Neuroprotective Agents
keywords: apoptosis; autophagy; damage-associated molecular pattern; high-mobility group B protein 1; necroptosis; necrosis; neuroinflammation; neurotrauma; pathogen-associated molecular pattern; thrombomodulin