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The intrinsic pathway of apoptosis (mitochondrial apoptosis pathway) and abnormal mitochondrial fission and fusion have a detrimental effect on cells under a variety of intracellular stresses including hypoxia, oxidative stress, drug toxicity or\n                    <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content>\n                    damage and contributes to the development of heart failure (\n                    <jats:styled-content style=\"fixed-case\">HF<\/jats:styled-content>\n                    ), myocardial infarction (\n                    <jats:styled-content style=\"fixed-case\">MI<\/jats:styled-content>\n                    ), diabetic cardiomyopathy and ischaemia\/reperfusion injury (I\/R). Micro\n                    <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                    s (mi\n                    <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                    s) are endogenous short non\u2010coding\n                    <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                    s, which target 3\u2032\u2010untranslated region of\n                    <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content>\n                    to switch off gene expression. They play crucial roles in regulating complicated cardiac signalling and transcriptional events during cardiac development as well as in diseased condition. In this review, we summarize the molecular mechanism of mitochondrial apoptosis in cardiac cells and influence of mi\n                    <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                    s on them. Mi\n                    <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>\n                    s regulate cardiac mitochondrial apoptosis by exert their effects on mitochondrial fission and fusion, reactive oxygen species (\n                    <jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>\n                    ) generation and Ca\n                    <jats:sup>2+<\/jats:sup>\n                    homeostasis, Bcl\u20102 family members, and other mitochondrial function proteins. This advancement in understanding mechanism of cardiac cells death provides us new therapy targets for cardiovascular diseases associated with mitochondrial dysfunctions.\n                  <\/jats:p>","DOI":"10.1111\/1440-1681.12720","type":"journal-article","created":{"date-parts":[[2016,12,24]],"date-time":"2016-12-24T12:05:22Z","timestamp":1482581122000},"page":"431-440","source":"Crossref","is-referenced-by-count":31,"title":["Effects of mi\n                    <scp>RNA<\/scp>\n                    s on myocardial apoptosis by modulating mitochondria related proteins"],"prefix":"10.1111","volume":"44","author":[{"given":"Yanfang","family":"Zhao","sequence":"first","affiliation":[{"name":"Centre for Developmental Cardiology Institute for Translational Medicine Qingdao University  Qingdao China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Murugavel","family":"Ponnusamy","sequence":"additional","affiliation":[{"name":"Centre for Developmental Cardiology Institute 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