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MtDNA decline, mitochondrial defects, and mitochondrial oxidative stress are now well recognized in a variety of diseases such as neurodegenerative diseases, diabetes mellitus, cancer, and even aging. The present study clarified the crucial role of mitochondrial transcription factor A (TFAM) in cardiovascular stress response. With further knowledge on the mechanisms of TFAM for maintenance of mtDNA copy number and mitochondrial function, it may eventually be possible to develop novel strategies for the treatment ofcardiovascular diseases including heart 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