Mitochondria provide energy for specialized functions at the cellular and organ level. The remarkable symbiotic relationship between mitochondria and the cell touches on every aspect of cell biology. Recent studies in mitochondrial biology have uncovered ways in which mitochondria affect human disease and have identified new targets for clinical intervention.
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References
Murphy, E. et al. Mitochondrial function, biology and role in disease: a Scientific Statement from the American Heart Association. Circ. Res. http://dx.doi.org/10.1161/RES.0000000000000104 (2016).
Bottomley, P. A. et al. Metabolic rates of ATP transfer through creatine kinase (CK flux) predict clinical heart failure events and death. Sci. Transl. Med. 5, 215re213 (2013).
Dey, S., Sidor, A. & O'Rourke, B. Compartment-specific control of reactive oxygen species scavenging by antioxidant pathway enzymes. J. Biol. Chem. 291, 11185–11197 (2016).
Snow, B. J. et al. A double-blind, placebo-controlled study to assess the mitochondria-targeted antioxidant MitoQ as a disease-modifying therapy in Parkinson's disease. Mov. Disord. 25, 1670–1674 (2010).
Chakrabarti, A. K. et al. Rationale and design of the EMBRACE STEMI study: a phase 2a, randomized, double-blind, placebo-controlled trial to evaluate the safety, tolerability and efficacy of intravenous Bendavia on reperfusion injury in patients treated with standard therapy including primary percutaneous coronary intervention and stenting for ST-segment elevation myocardial infarction. Am. Heart J. 165, 509–514.e7 (2013).
Huang, J. et al. Decreased peripheral mitochondrial DNA copy number is associated with the risk of heart failure and long-term outcomes. Medicine (Baltimore) 95, e3323 (2016).
Feuer, W. J. et al. Gene therapy for leber hereditary optic neuropathy: initial results. Ophthalmology 123, 558–570 (2016).
Hardiville, S. & Hart, G. W. Nutrient regulation of signaling, transcription, and cell physiology by O-GlcNAcylation. Cell Metab. 20, 208–213 (2014).
Ide, T. et al. Mitochondrial DNA damage and dysfunction associated with oxidative stress in failing hearts after myocardial infarction. Circ. Res. 88, 529–535 (2001).
West, A. P. et al. Mitochondrial DNA stress primes the antiviral innate immune response. Nature 520, 553–557 (2015).
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Supported by NIH/NHLBI grants R01HL108917 and R37HL54598.
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O'Rourke, B. Beyond the power of mitochondria. Nat Rev Cardiol 13, 386–388 (2016). https://doi.org/10.1038/nrcardio.2016.95
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DOI: https://doi.org/10.1038/nrcardio.2016.95
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