{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T06:34:06Z","timestamp":1790836446203,"version":"4.1.0"},"reference-count":45,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2023,2,23]],"date-time":"2023-02-23T00:00:00Z","timestamp":1677110400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Diabetes Invest"],"published-print":{"date-parts":[[2023,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims\/Introduction<\/jats:title>\n                    <jats:p>\n                      We previously showed that upregulation of myocardial adenosine monophosphate deaminase (AMPD) is associated with pressure overload\u2010induced diastolic dysfunction in type\u20092 diabetes hearts. Here, we examined involvement of AMPD localized in the endoplasmic reticulum\u2013mitochondria interface in mitochondrial Ca\n                      <jats:sup>2+<\/jats:sup>\n                      overload and its pathological significance.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and Methods<\/jats:title>\n                    <jats:p>We used type\u20092 diabetes Otsuka Long\u2013Evans Tokushima Fatty rats (OLETF) and non\u2010diabetes Long\u2013Evans Tokushima Otsuka Fatty rats (LETO) as well as AMPD3\u2010overexpressing H9c2 cells and human embryonic kidney\u2009293 cells.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      OLETF, but not LETO, showed diastolic dysfunction under the condition of phenylephrine\u2010induced pressure overload. The levels of 90\u2010kDa AMPD3 in outer mitochondrial membranes\/endoplasmic reticulum and mitochondria\u2010associated endoplasmic reticulum membrane (MAM) fractions were significantly higher in OLETF than in LETO. The area of the MAM quantified by electron microscopic analysis was 57% larger, mitochondrial Ca\n                      <jats:sup>2+<\/jats:sup>\n                      level under the condition of pressure overload was 47% higher and Ca\n                      <jats:sup>2+<\/jats:sup>\n                      retention capacity in MAM\u2010containing crude mitochondria isolated before the pressure overloading was 21% lower in OLETF than in LETO (all\n                      <jats:italic>P<\/jats:italic>\n                      \u2010values &lt;0.05). Transfection of FLAG\u2010AMPD3 in cells resulted in significant enlargement of the MAM area, and impairment in pyruvate\/malate\u2010driven adenosine triphosphate\u2010stimulated and uncoupler\u2010stimulated mitochondrial respiration compared with those in control cells.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      The findings suggest that 90\u2010kDa AMPD3 localized in the endoplasmic reticulum\u2013mitochondria interface promotes formation of the MAM, inducing mitochondrial Ca\n                      <jats:sup>2+<\/jats:sup>\n                      overload and dysfunction in type\u20092 diabetes hearts.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jdi.13982","type":"journal-article","created":{"date-parts":[[2023,2,23]],"date-time":"2023-02-23T03:45:29Z","timestamp":1677123929000},"page":"560-569","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Adenosine monophosphate deaminase in the endoplasmic reticulum\u2013mitochondria interface promotes mitochondrial Ca\n                    <sup>2+<\/sup>\n                    overload in type\u20092 diabetes rat hearts"],"prefix":"10.1111","volume":"14","author":[{"given":"Arata","family":"Osanami","sequence":"first","affiliation":[{"name":"Department of Cardiovascular, Renal and Metabolic Medicine Sapporo Medical University School of Medicine  Sapporo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7876-1772","authenticated-orcid":false,"given":"Tatsuya","family":"Sato","sequence":"additional","affiliation":[{"name":"Department of 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