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High energy\u2010demanding organs, such as heart, are usually involved in mitochondria diseases. However, whether and how m.3243A&gt;G affects cardiomyocytes remain unknown. We have established patient\u2010specific iPSCs carrying m.3243A&gt;G and induced cardiac differentiation. Cardiomyocytes with high m.3243A&gt;G burden exhibited hypertrophic phenotype. This point mutation is localised in\n                    <jats:italic>MT\u2010TL1<\/jats:italic>\n                    encoding tRNA\n                    <jats:sup>Leu (UUR)<\/jats:sup>\n                    . m.3243A&gt;G altered tRNA\n                    <jats:sup>Leu (UUR)<\/jats:sup>\n                    conformation and decreased its stability. mtDNA is essential for mitochondrial function. Mitochondria dysfunction occurred and tended to become round. Its interaction with ER, mitochondria\u2010associated ER membrane (MAM), was disrupted with decreased contact number and length. MAM is a central hub for calcium trafficking. Disrupted MAM disturbed calcium homeostasis, which may be the direct and leading cause of cardiomyocyte hypertrophy, as MAM enforcement reversed this pathological state. Considering the threshold effect of mitochondrial disease, mito\u2010TALENs were introduced to eliminate mutant mitochondria and release mutation load. Mutation reduction partially reversed the cellular behaviour and made it approach to that of control one. These findings reveal the pathogenesis underlying m.3243A&gt;G from perspective of organelle interaction, rather than organelle. Beyond mitochondria quality control, its proper interaction with other organelles, such as ER, matters for mitochondria disease. This study may provide inspiration for mitochondria disease intervention.\n                  <\/jats:p>","DOI":"10.1111\/cpr.70002","type":"journal-article","created":{"date-parts":[[2025,2,21]],"date-time":"2025-02-21T08:08:59Z","timestamp":1740125339000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Mitochondrial Mutation Leads to Cardiomyocyte Hypertrophy by Disruption of Mitochondria\u2010Associated\n                    <scp>ER<\/scp>\n                    Membrane"],"prefix":"10.1111","volume":"58","author":[{"given":"Miao","family":"Yu","sequence":"first","affiliation":[{"name":"Department of Cardiovascular Surgery of the First Affiliated Hospital &amp; Institute for Cardiovascular Science, Collaborative Innovation Center of Hematology, State Key Laboratory of Radiation Medicine and Protection, Suzhou Medical College Soochow University  Suzhou Jiangsu 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