Accordingly, cardiac myocytes require a specialized, high-capacity mitochondrial system. High energy demands of the postnatal heart are largely satisfied by ATP generated via mitochondrial oxidative phosphorylation (OXPHOS). However, transcriptional profiling demonstrated that PGC-1 coactivators are required for high-level expression of nuclear- and mitochondrial-encoded genes involved in mitochondrial dynamics and energy transduction in the adult heart. Surprisingly, PGC-1α/β deficiency in the adult heart did not result in evidence of abnormal mitochondrial dynamics or heart failure. PGC-lα was shown to directly regulate Mfn1 gene transcription by coactivating the estrogen-related receptor α on a conserved DNA element. The expression of genes involved in mitochondrial fusion ( Mfn1, Opa1) and fission ( Drp1, Fis1) was altered in the hearts of PGC-1α/β–deficient mice. Marked mitochondrial structural derangements were observed in hearts of PGC-1α/β–deficient mice during postnatal growth, including fragmentation and elongation, associated with the development of a lethal cardiomyopathy. Customer Service and Ordering InformationĬonditional gene targeting was used in mice to explore the role of PGC-1 coactivators during postnatal cardiac development and in adult hearts.Stroke: Vascular and Interventional Neurology.Journal of the American Heart Association (JAHA).Circ: Cardiovascular Quality & Outcomes.Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB).Continued abuse of our services will cause your IP address to be blocked indefinitely. Please fill out the CAPTCHA below and then click the button to indicate that you agree to these terms. If you wish to be unblocked, you must agree that you will take immediate steps to rectify this issue. If you do not understand what is causing this behavior, please contact us here. If you promise to stop (by clicking the Agree button below), we'll unblock your connection for now, but we will immediately re-block it if we detect additional bad behavior.
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