Neural Regeneration Research ›› 2021, Vol. 16 ›› Issue (3): 482-488.doi: 10.4103/1673-5374.290097

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Connexin therapeutics: blocking connexin hemichannel pores is distinct from blocking pannexin channels or gap junctions 

Monica L. Acosta1, 5, 6, 7, *, Mohd N. Mat Nor1, 2, Cindy X. Guo1, Odunayo O. Mugisho3, 4, 5, Frazer P. Coutinho3, Ilva D. Rupenthal3, 4, 5, Colin R. Green3, 5   

  1. 1 School of Optometry and Vision Science, University of Auckland, Auckland, New Zealand;  2 Faculty of Medicine, Universiti Sultan Zainal Abidin, Terengganu, Malaysia;  3 Department of Ophthalmology, University of Auckland, Auckland, New Zealand;  4 Buchanan Ocular Therapeutics Unit, Department of Ophthalmology, Auckland, New Zealand;  5 New Zealand National Eye Centre, University of Auckland, Auckland, New Zealand;  6 Centre for Brain Research, Faculty of Medical and Health Sciences, The University of Auckland, Auckland, New Zealand;  7 Brain Research New Zealand–Rangahau Roro Aotearoa, Auckland, New Zealand
  • Online:2021-03-15 Published:2020-12-17
  • Contact: Monica L. Acosta, PhD, m.acosta@auckland.ac.nz.
  • Supported by:
    This work was supported in part by New Zealand Lottery Health Research, the Maurice and Phyllis Paykel Trust and the New Zealand Optometric Vision Research Foundation.

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Abstract: Compounds that block the function of connexin and pannexin protein channels have been suggested to be valuable therapeutics for a range of diseases. Some of these compounds are now in clinical trials, but for many of them, the literature is inconclusive about the molecular effect on the tissue, despite evidence of functional recovery. Blocking the different channel types has distinct physiological and pathological implications and this review describes current knowledge of connexin and pannexin protein channels, their function as channels and possible mechanisms of the channel block effect for the latest therapeutic compounds. We summarize the evidence implicating pannexins and connexins in disease, considering their homeostatic versus pathological roles, their contribution to excesive ATP release linked to disease onset and progression.

Key words: connexin, gap junction, gap19, hemichannel, pannexin, retina, tonabersat