Scientific article

Gap junctional communication in tissue inflammation and repair

Published inBiochimica et biophysica acta, vol. 1711, no. 2, p. 197-207
Publication date2005

Local injury induces a complex orchestrated response to stimulate healing of injured tissues, cellular regeneration and phagocytosis. Practically, inflammation is defined as a defense process whereby fluid and white blood cells accumulate at a site of injury. The balance of cytokines, chemokines, and growth factors is likely to play a key role in regulating important cell functions such as migration, proliferation, and matrix synthesis during the process of inflammation. Hence, the initiation, maintenance, and resolution of innate responses depend upon cellular communication. A process similar to tissue repair and subsequent scarring is found in a variety of fibrotic diseases. This may occur in a single organ such as liver, kidneys, pancreas, lung, skin, and heart, but fibrosis may also have a more generalized distribution such as in atherosclerosis. The purpose of this review is to summarize recent advances on the contribution of gap junction-mediated intercellular communication in the modulation of the inflammatory response and tissue repair.

  • Animals
  • Cell Communication/physiology
  • Chemokines/biosynthesis
  • Connexins/physiology
  • Cytokines/biosynthesis
  • Gap Junctions/physiology
  • Homeostasis/physiology
  • Humans
  • Immunity
  • Inflammation/physiopathology
  • Wound Healing/physiology
Citation (ISO format)
CHANSON, Marc et al. Gap junctional communication in tissue inflammation and repair. In: Biochimica et biophysica acta, 2005, vol. 1711, n° 2, p. 197–207. doi: 10.1016/j.bbamem.2004.10.005
Main files (1)
Article (Published version)
ISSN of the journal0006-3002

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