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Non\u2010responsiveness to IPoC possibly caused by co\u2010morbidities limits its clinical attractiveness. We analysed differences in the expression of mitochondrial proteins between IPoC responder (IPoC\u2010R) and non\u2010responder (IPoC\u2010NR). Eighty rats were randomly grouped to sham, ischaemia\/reperfusion (I\/R), IPoC or ischaemic pre\u2010conditioning (IPC, as positive cardioprotective intervention) in vivo. Infarct sizes were quantified by plasma troponin I levels 60\u00a0minutes after reperfusion. After 7\u00a0days, rats were sacrificed and left ventricular tissue was taken for post hoc analysis. The transcriptome was analysed by qRT\u2010PCR and small RNA sequencing. Key findings were verified by immunoblots. I\/R increased plasma troponin I levels compared to Sham. IPC reduced troponin I compared to I\/R, whereas IPoC produced either excellent protection (IPoC\u2010R) or no protection (IPoC\u2010NR). Twenty\u2010one miRs were up\u2010regulated by I\/R and modified by IPoC. qRT\u2010PCR analysis revealed that IPoC\u2010R differed from other groups by reduced expression of arginase\u20102 and bax, whereas the mitochondrial uncoupling protein (UCP)\u20102 was induced in IPC and IPoC\u2010R. IPoC\u2010R and IPoC\u2010NR synergistically increased the expression of non\u2010mitochondrial proteins like VEGF and SERCA2a independent of the infarct size. Cardiac function was more closely linked to differences in mitochondrial proteins than on regulation of calcium\u2010handling proteins. In conclusion, healthy rats could not always be protected by IPoC. IPoC\u2010NR displayed an incomplete responsiveness which is reflected by different changes in the mitochondrial transcriptome compared to IPoC\u2010R. This study underlines the importance of mitochondrial proteins for successful long\u2010term outcome.<\/jats:p>","DOI":"10.1111\/jcmm.15209","type":"journal-article","created":{"date-parts":[[2020,4,16]],"date-time":"2020-04-16T09:41:38Z","timestamp":1587030098000},"page":"5528-5541","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":20,"title":["Ischaemic post\u2010conditioning in rats: Responder and non\u2010responder differ in transcriptome of mitochondrial proteins"],"prefix":"10.1111","volume":"24","author":[{"given":"Rolf","family":"Schreckenberg","sequence":"first","affiliation":[{"name":"Department of Physiology Justus Liebig\u2010University Gie\u00dfen Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Johann","family":"Klein","sequence":"additional","affiliation":[{"name":"Department of Physiology Justus Liebig\u2010University Gie\u00dfen Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hanna Sarah","family":"Kutsche","sequence":"additional","affiliation":[{"name":"Department of Physiology Justus Liebig\u2010University Gie\u00dfen Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rainer","family":"Schulz","sequence":"additional","affiliation":[{"name":"Department of Physiology Justus Liebig\u2010University Gie\u00dfen Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kamilla","family":"G\u00f6m\u00f6ri","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Pharmacotherapy University of Szeged Szeged Hungary"},{"name":"Pharmahungary Group Szeged Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1936-6232","authenticated-orcid":false,"given":"P\u00e9ter","family":"Bencsik","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Pharmacotherapy University of Szeged Szeged Hungary"},{"name":"Pharmahungary Group Szeged Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bettina","family":"Benczik","sequence":"additional","affiliation":[{"name":"Cardiometabolic and MTA-SE System Pharmacology Research Group Department of Pharmacology and Pharmacotherapy Semmelweis University Budapest Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bence","family":"\u00c1gg","sequence":"additional","affiliation":[{"name":"Pharmahungary Group Szeged Hungary"},{"name":"Cardiometabolic and MTA-SE System Pharmacology Research Group Department of Pharmacology and Pharmacotherapy Semmelweis University Budapest Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"\u00c9va","family":"S\u00e1ghy","sequence":"additional","affiliation":[{"name":"Cardiometabolic and MTA-SE System Pharmacology Research Group Department of Pharmacology and Pharmacotherapy Semmelweis University Budapest Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P\u00e9ter","family":"Ferdinandy","sequence":"additional","affiliation":[{"name":"Pharmahungary Group Szeged Hungary"},{"name":"Cardiometabolic and MTA-SE System Pharmacology Research Group Department of Pharmacology and Pharmacotherapy Semmelweis University Budapest Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6093-4919","authenticated-orcid":false,"given":"Klaus\u2010Dieter","family":"Schl\u00fcter","sequence":"additional","affiliation":[{"name":"Department of Physiology Justus Liebig\u2010University Gie\u00dfen Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2020,4,16]]},"reference":[{"key":"e_1_2_9_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jchf.2017.09.015"},{"key":"e_1_2_9_3_1","doi-asserted-by":"publisher","DOI":"10.1136\/heartjnl-2015-307804"},{"key":"e_1_2_9_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2018.09.086"},{"key":"e_1_2_9_5_1","doi-asserted-by":"publisher","DOI":"10.1124\/pr.113.008300"},{"key":"e_1_2_9_6_1","doi-asserted-by":"publisher","DOI":"10.1093\/cvr\/cvx049"},{"key":"e_1_2_9_7_1","doi-asserted-by":"publisher","DOI":"10.33549\/physiolres.932981"},{"key":"e_1_2_9_8_1","doi-asserted-by":"publisher","DOI":"10.1080\/14017430601007587"},{"key":"e_1_2_9_9_1","first-page":"521","article-title":"Very short cycles of postconditioning have no protective effect against reperfusion injury. 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