Abstract
Gap junctions and connexin hemichannels mediate intercellular and extracellular communication, respectively. While gap junctions are seen as the “good guys” by controlling homeostasis, connexin hemichannels are considered as the “bad guys”, as their activation is associated with the onset and dissemination of disease. Open connexin hemichannels indeed mediate the transport of messengers between the cytosol and extracellular environment and, by doing so, fuel inflammation and cell death in a plethora of diseases. The present mini-review discusses the mechanisms involved in the activation of connexin hemichannels during pathology.
Highlights
Connexins have been detected in virtually all cell types and organs
Connexin hemichannels become predominantly active in pathological conditions, and support inflammation and cell death
Since gap junctions and connexin hemichannels are composed of the same connexin building blocks and allow the passage of identical molecules and ions, it is difficult to distinguish between both channel types
Summary
Cell plasma membrane transport proteins include different membrane proteins that enable such transfer Among those are gap junctions, which form cell-to-cell junctions that facilitate direct intercellular communication between cells by allowing the passage of small and hydrophilic molecules, including glucose, glutamate, glutathione, adenosine triphosphate (ATP), cyclic adenosine monophosphate, inositol triphosphate and ions, such as calcium, sodium and potassium [1]. These communicating cell-to-cell junctions serve as gatekeepers for many physiological processes [2,3] They arise from the interaction of two hemichannels, which in turn are built up by six connexin proteins at the cell plasma membrane surface of adjacent cells. Over the past two decades, it has become clear that connexin hemichannels provide an autonomous communication pathway for communication on their own, independent of their role as structural precursors of gap junctions [4].
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