|Cancer||Cell death||Cell cycle||Cytoskeleton||Exo/endocytosis||Differentiation||Division||Organelles||Signalling||Stem cells||Trafficking|
Cell Biology International (2008) 32, 15781583 (Printed in Great Britain)
Interrupting the inflammatory cycle in chronic diseases – Do gap junctions provide the answer?
Colin R. Green* and Louise F.B. Nicholson
Faculty of Medical and Health Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand
A number of chronic diseases, including neurodegenerative, cardiovascular and metabolic disorders, are associated with genetic susceptibility. Some may originate on exposure to an environmental stimulus. Regardless of genetic predisposition or external stimulus, these chronic diseases, once triggered, share an inflammatory component making them effectively persistent “wounds”. There is also increasing evidence that the presence of one disease can cause activation of another apparently unrelated disease, leading to multiple disorders via activation of an immune response that ‘fast forwards’ disease progression. Here we review common aspects of a number of chronic disease conditions, and put forward the proposal that gap junction modulation may provide an opportunity to break the inflammatory cycle that sustains and links these disorders.
Key words: Connexin, Neurodegenerative disease, Cardiovascular disease, Parkinson's, Huntington's, Alzheimer's, Epilepsy, Diabetes, Obesity, Chronic inflammation, Inflammatory cytokines, Gap junctions.
Received 16 September 2008; accepted 22 September 2008doi:10.1016/j.cellbi.2008.09.006