{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T22:17:46Z","timestamp":1790201866289,"version":"4.1.0"},"reference-count":46,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2017,3]]},"abstract":"<jats:sec xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">The cardiac microvascular system ischemia\/reperfusion injury following percutaneous coronary intervention is a clinical thorny problem. This study explores the mechanisms by which ischemia\/reperfusion injury induces cardiac microcirculation collapse.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Methods and Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              In wild\u2010type mice, mitochondrial fission factor (Mff) expression increased in response to acute microvascular ischemia\/reperfusion injury. Compared with wild\u2010type mice, homozygous Mff\u2010deficient (Mff\n              <jats:sup>gt<\/jats:sup>\n              ) mice exhibited a smaller infarcted area, restored cardiac function, improved blood flow, and reduced microcirculation perfusion defects. Histopathology analysis demonstrated that cardiac microcirculation endothelial cells (\n              <jats:styled-content style=\"fixed-case\">CMECs<\/jats:styled-content>\n              ) in Mff\n              <jats:sup>gt<\/jats:sup>\n              mice had an intact endothelial barrier, recovered phospho\u2010endothelial nitric oxide synthase production, opened lumen, undivided mitochondrial structures, and less\n              <jats:styled-content style=\"fixed-case\">CMEC<\/jats:styled-content>\n              death. In vitro, Mff\u2010deficient\n              <jats:styled-content style=\"fixed-case\">CMEC<\/jats:styled-content>\n              s (derived from Mff\n              <jats:sup>gt<\/jats:sup>\n              mice or Mff small interfering RNA\u2013treated) demonstrated less mitochondrial fission and mitochondrial\u2010dependent apoptosis compared with cells derived from wild\u2010type mice. The loss of Mff inhibited mitochondrial permeability transition pore opening via blocking the oligomerization of voltage\u2010dependent anion channel 1 and subsequent hexokinase 2 separation from mitochondria. Moreover, Mff deficiency reduced the cyt\u2010c leakage into the cytoplasm by alleviating cardiolipin oxidation resulting from damage to the electron transport chain complexes and mitochondrial reactive oxygen species overproduction.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">This evidence clearly illustrates that microcirculatory ischemia\/reperfusion injury can be attributed to Mff\u2010dependent mitochondrial fission via voltage\u2010dependent anion channel 1\/hexokinase 2\u2013mediated mitochondrial permeability transition pore opening and mitochondrial reactive oxygen species\/cardiolipin involved cyt\u2010c release.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/jaha.116.005328","type":"journal-article","created":{"date-parts":[[2017,3,14]],"date-time":"2017-03-14T00:20:32Z","timestamp":1489450832000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":269,"title":["Mff\u2010Dependent Mitochondrial Fission Contributes to the Pathogenesis of Cardiac Microvasculature Ischemia\/Reperfusion Injury via Induction of mROS\u2010Mediated Cardiolipin Oxidation and HK2\/VDAC1 Disassociation\u2010Involved mPTP Opening"],"prefix":"10.1161","volume":"6","author":[{"given":"Hao","family":"Zhou","sequence":"first","affiliation":[{"name":"Department of Cardiology Chinese PLA General Hospital Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shunying","family":"Hu","sequence":"additional","affiliation":[{"name":"Department of Cardiology Chinese PLA General Hospital Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qinhua","family":"Jin","sequence":"additional","affiliation":[{"name":"Department of Cardiology Chinese PLA General Hospital Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chen","family":"Shi","sequence":"additional","affiliation":[{"name":"Department of Radiation Oncology Peking University Cancer Hospital and Institute Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ying","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Cardiology Chinese PLA General Hospital Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pingjun","family":"Zhu","sequence":"additional","affiliation":[{"name":"Department of Cardiology Chinese PLA General Hospital Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiang","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Cardiology Chinese PLA General Hospital Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Feng","family":"Tian","sequence":"additional","affiliation":[{"name":"Department of Cardiology Chinese PLA General Hospital Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yundai","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Cardiology Chinese PLA General Hospital Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_1_2_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI107898"},{"key":"e_1_3_1_3_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.RES.66.4.986"},{"key":"e_1_3_1_4_2","doi-asserted-by":"publisher","DOI":"10.1038\/ncpcardio0632"},{"key":"e_1_3_1_5_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCIMAGING.109.897439"},{"key":"e_1_3_1_6_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev-physiol-030212-183804"},{"key":"e_1_3_1_7_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF00223424"},{"key":"e_1_3_1_8_2","first-page":"H689","article-title":"Energetic response of coronary endothelial cells to hypoxia","volume":"258","author":"Mertens S","year":"1990","unstructured":"Mertens S, Noll T, Spahr R, Krutzfeldt A, Piper HM. 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