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However, the relationship between the autophagy machinery and Na\n                    <jats:sup>+<\/jats:sup>\n                    ,K\n                    <jats:sup>+<\/jats:sup>\n                    -ATPase is unknown. We explored the hypothesis that Na\n                    <jats:sup>+<\/jats:sup>\n                    ,K\n                    <jats:sup>+<\/jats:sup>\n                    -ATPase interacts with the autophagy protein Beclin 1 during stress and autosis-inducing conditions. Starvation increased the Beclin 1\/Na\n                    <jats:sup>+<\/jats:sup>\n                    ,K\n                    <jats:sup>+<\/jats:sup>\n                    -ATPase interaction in cultured cells, and this was blocked by cardiac glycosides, inhibitors of Na\n                    <jats:sup>+<\/jats:sup>\n                    ,K\n                    <jats:sup>+<\/jats:sup>\n                    -ATPase. Increases in Beclin 1\/Na\n                    <jats:sup>+<\/jats:sup>\n                    ,K\n                    <jats:sup>+<\/jats:sup>\n                    -ATPase interaction were also observed in tissues from starved mice, livers of patients with anorexia nervosa, brains of neonatal rats subjected to cerebral hypoxia-ischemia (HI), and kidneys of mice subjected to renal ischemia\/reperfusion injury (IRI). Cardiac glycosides blocked the increased Beclin 1\/Na\n                    <jats:sup>+<\/jats:sup>\n                    ,K\n                    <jats:sup>+<\/jats:sup>\n                    -ATPase interaction during cerebral HI injury and renal IRI. In the mouse renal IRI model, cardiac glycosides reduced numbers of autotic cells in the kidney and improved clinical outcome. Moreover, blockade of endogenous cardiac glycosides increased Beclin 1\/Na\n                    <jats:sup>+<\/jats:sup>\n                    ,K\n                    <jats:sup>+<\/jats:sup>\n                    -ATPase interaction and autotic cell death in mouse hearts during exercise. Thus, Beclin 1\/Na\n                    <jats:sup>+<\/jats:sup>\n                    ,K\n                    <jats:sup>+<\/jats:sup>\n                    -ATPase interaction is increased in stress conditions, and cardiac glycosides decrease this interaction and autosis in both pathophysiological and physiological settings. This crosstalk between cellular machinery that generates and consumes energy during stress may represent a fundamental homeostatic mechanism.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.133282","type":"journal-article","created":{"date-parts":[[2020,1,15]],"date-time":"2020-01-15T11:04:11Z","timestamp":1579086251000},"source":"Crossref","is-referenced-by-count":56,"title":["Interaction between the autophagy protein Beclin 1 and Na+,K+-ATPase during starvation, exercise, and ischemia"],"prefix":"10.1172","volume":"5","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7704-4285","authenticated-orcid":true,"given":"\u00c1lvaro F.","family":"Fern\u00e1ndez","sequence":"first","affiliation":[{"name":"Center for Autophagy Research,"},{"name":"Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, 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