of telomeres and TERT that comes with aging has been associated with impaired mitochondrial biogenesis. AMPK expression has also been shown to diminish with age, which may also contribute to suppressing mitochondrial biogenesis. Clinical Applications of Targeting Mitochondrial Biogenesis Mitochondrial biogenesis can be targeted to prevent cancer proliferation. Specifically, two biogenesis regulators—PGC1α and c-Myc—can be targeted to prevent cancer proliferation. PGC1α is a key component in mitochondrial biogenesis—as a transcriptional coactivator, it targets multiple transcription factors and the estrogen-related receptor alpha (ERRα). Compounds that target the pathway between PGC1α and ERRα, such as the ERRα inverse agonist, XCT-790, have been found to significantly decrease mitochondrial biogenesis, thus greatly reducing cancer cells’ proliferation and increasing their sensitivity to chemotherapeutic agents. c-Myc, a transcription factor, can be inhibited during its dimerization with Max protein by molecules such as IIA6B17 and omomyc. Inhibition of the c-Myc-Max complex can block the cell cycle and induce apoptosis in cancer cells. References Further reading Cell biology