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The large-conductance calcium-activated K<jats:sup>+<\/jats:sup> channels (BK) are thus interesting candidates to protect against excess calcium influx and the events leading to ischemic injury. Indeed, the mitochondrial BK channels (mitoBK) have recently been shown to play a protective function against ischemia-reperfusion injury both in vitro and in animal models, although the exact mechanism of this protection is still under scrutiny. In addition, in both the plasma membrane and mitochondrial BK channel, the \u03b1-subunit itself is sensitive to hypoxia. This sensitivity is tissue specific and conferred by a highly conserved motif within an alternatively spliced cysteine-rich insert (STREX) in the intracellular C terminus of the channel. This review describes recent developments of the increasing relevance of BK channels in hypoxia and ischemia-reperfusion injury. <\/jats:p>","DOI":"10.1152\/ajpheart.00319.2014","type":"journal-article","created":{"date-parts":[[2014,7,12]],"date-time":"2014-07-12T02:53:59Z","timestamp":1405133639000},"page":"H811-H817","source":"Crossref","is-referenced-by-count":22,"title":["Hypoxia and ischemia-reperfusion: a B<sub>i<\/sub>K contribution?"],"prefix":"10.1152","volume":"307","author":[{"given":"Jean-Yves","family":"Tano","sequence":"first","affiliation":[{"name":"Experimental and Clinical Research Center (a Joint Institution Between the Charit\u00e9 University Medicine and Max Delbr\u00fcck Center for Molecular Medicine), Berlin-Buch, Germany; and Nephrology\/Intensive Care Section, Charit\u00e9 Campus Virchow, Berlin, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maik","family":"Gollasch","sequence":"additional","affiliation":[{"name":"Experimental and 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