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Despite successful reperfusion therapy, ischaemia reperfusion injury (IRI) can induce oxidative stress (OS), cardiomyocyte apoptosis, autophagy and release of inflammatory cytokines, resulting in increased infarct size. In IRI, mitochondrial dysfunction is a key factor, which involves the production of reactive oxygen species, activation of inflammatory signalling cascades or innate immune responses, and apoptosis. Therefore, intercellular mitochondrial transfer could be considered as a promising treatment strategy for ischaemic heart disease. However, low transfer efficiency is a challenge in clinical settings. We previously reported uptake of isolated exogenous mitochondria into cultured cells through co\u2010incubation, mediated by macropinocytosis. Here, we report the use of transactivator of transcription dextran complexes (TAT\u2010dextran) to enhance cellular uptake of exogenous mitochondria and improve the protective effect of mitochondrial replenishment in neonatal rat cardiomyocytes (NRCMs) against OS. TAT\u2010dextran\u2013modified mitochondria (TAT\u2010Mito) showed a significantly higher level of cellular uptake. Mitochondrial transfer into NRCMs resulted in anti\u2010apoptotic capability and prevented the suppression of oxidative phosphorylation in mitochondria after OS. Furthermore, TAT\u2010Mito significantly reduced the apoptotic rates of cardiomyocytes after OS, compared to simple mitochondrial transfer. These results indicate the potential of mitochondrial replenishment therapy in OS\u2010induced myocardial IRI.<\/jats:p>","DOI":"10.1111\/jcmm.15120","type":"journal-article","created":{"date-parts":[[2020,3,25]],"date-time":"2020-03-25T05:41:09Z","timestamp":1585114869000},"page":"5007-5020","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":60,"title":["TAT\u2010dextran\u2013mediated mitochondrial transfer enhances recovery from models of reperfusion injury in cultured cardiomyocytes"],"prefix":"10.1111","volume":"24","author":[{"given":"Hideki","family":"Maeda","sequence":"first","affiliation":[{"name":"Department of Cardiovascular Medicine Graduate School of Medical Science Kyoto Prefectural University of Medicine Kyoto Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daisuke","family":"Kami","sequence":"additional","affiliation":[{"name":"Department of Regenerative Medicine Graduate School of Medical 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