{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T00:53:51Z","timestamp":1791161631629,"version":"4.1.0"},"reference-count":175,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2021,12,9]],"date-time":"2021-12-09T00:00:00Z","timestamp":1639008000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cardiovasc. Med."],"abstract":"<jats:p>Ischemic heart disease refers to myocardial degeneration, necrosis, and fibrosis caused by coronary artery disease. It can lead to severe left ventricular dysfunction (LVEF \u2264 35\u201340%) and is a major cause of heart failure (HF). In each contraction, myocardium is subjected to a variety of mechanical forces, such as stretch, afterload, and shear stress, and these mechanical stresses are clinically associated with myocardial remodeling and, eventually, cardiac outcomes. Mitochondria produce 90% of ATP in the heart and participate in metabolic pathways that regulate the balance of glucose and fatty acid oxidative phosphorylation. However, altered energetics and metabolic reprogramming are proved to aggravate HF development and progression by disturbing substrate utilization. This review briefly summarizes the current insights into the adaptations of cardiomyocytes to mechanical stimuli and underlying mechanisms in ischemic heart disease, with focusing on mitochondrial metabolism. We also discuss how mechanical circulatory support (MCS) alters myocardial energy metabolism and affects the detrimental metabolic adaptations of the dysfunctional myocardium.<\/jats:p>","DOI":"10.3389\/fcvm.2021.789267","type":"journal-article","created":{"date-parts":[[2021,12,9]],"date-time":"2021-12-09T06:17:50Z","timestamp":1639030670000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":59,"title":["Mitochondrial Metabolism in Myocardial Remodeling and Mechanical Unloading: Implications for Ischemic Heart Disease"],"prefix":"10.3389","volume":"8","author":[{"given":"Min","family":"Jiang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoye","family":"Xie","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Feng","family":"Cao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yabin","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2021,12,9]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"5375","DOI":"10.1161\/CIRCOUTCOMES.118.005375","article-title":"Mortality from ischemic heart disease","volume":"12","author":"Nowbar","year":"2019","journal-title":"Circulation"},{"key":"B2","doi-asserted-by":"publisher","first-page":"1463","DOI":"10.1161\/CIRCULATIONAHA.118.031373","article-title":"Reappraisal of ischemic heart disease","volume":"138","author":"Kaski","year":"2018","journal-title":"Circulation."},{"key":"B3","doi-asserted-by":"publisher","first-page":"634","DOI":"10.1016\/j.ehj.2004.02.018","article-title":"Metabolic manipulation in ischaemic heart disease, a novel approach to treatment","volume":"25","author":"Lee","year":"2004","journal-title":"Eur Heart J."},{"key":"B4","doi-asserted-by":"publisher","first-page":"1487","DOI":"10.1161\/CIRCRESAHA.121.318241","article-title":"Cardiac energy metabolism in heart failure","volume":"128","author":"Lopaschuk","year":"2021","journal-title":"Circ Res."},{"key":"B5","doi-asserted-by":"publisher","first-page":"1765","DOI":"10.1016\/j.ehj.2004.08.019","article-title":"Metabolic therapy for heart failure","volume":"25","author":"Faadielessop","year":"2004","journal-title":"Eur Heart J."},{"key":"B6","doi-asserted-by":"publisher","first-page":"207","DOI":"10.1152\/physrev.00015.2009","article-title":"Myocardial fatty acid metabolism in health and disease","volume":"90","author":"Lopaschuk","year":"2010","journal-title":"Physiol Rev."},{"key":"B7","doi-asserted-by":"publisher","first-page":"1681","DOI":"10.1161\/01.RES.68.6.1681","article-title":"Effect of increasing degrees of ischemic injury on myocardial oxidative metabolism early after reperfusion in isolated rat hearts","volume":"68","author":"Gorge","year":"1991","journal-title":"Circ Res."},{"key":"B8","doi-asserted-by":"publisher","first-page":"5937","DOI":"10.1111\/jcmm.15180","article-title":"Cardiac metabolism as a driver and therapeutic target of myocardial infarction","volume":"24","author":"Zuurbier","year":"2020","journal-title":"J Cell Mol Med."},{"key":"B9","doi-asserted-by":"publisher","first-page":"908","DOI":"10.1007\/s00424-001-0744-2","article-title":"Post-ischaemic changes in the response time of oxygen consumption to demand in the isolated rat heart are mediated partly by calcium and glycolysis","volume":"443","author":"Zuurbier","year":"2002","journal-title":"Pflugers Arch."},{"key":"B10","doi-asserted-by":"publisher","first-page":"567","DOI":"10.1161\/01.RES.71.3.567","article-title":"Dissociation between contractile function and oxidative metabolism in postischemic myocardium. 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