Carlos T Moraes


Affiliation: University of Miami
Country: USA


  1. Lima P, Pereira C, Nissanka N, Arguello T, Gavini G, Maranduba C, et al. Photobiomodulation enhancement of cell proliferation at 660 nm does not require cytochrome c oxidase. J Photochem Photobiol B. 2019;194:71-75 pubmed publisher
    ..These results showed that although metabolic changes are associated with PBM, CCO is not required for its cell proliferation enhancing effect. ..
  2. Nissanka N, Minczuk M, Moraes C. Mechanisms of Mitochondrial DNA Deletion Formation. Trends Genet. 2019;35:235-244 pubmed publisher
    ..We propose that mtDNA deletions formed from replication errors versus following double-strand breaks can be mediated by separate pathways. ..
  3. Arguello T, Köhrer C, RajBhandary U, Moraes C. Mitochondrial methionyl N-formylation affects steady-state levels of oxidative phosphorylation complexes and their organization into supercomplexes. J Biol Chem. 2018;293:15021-15032 pubmed publisher
    ..In summary, N-formylation is not essential for mitochondrial protein synthesis but is critical for efficient synthesis of several mitochondrially encoded peptides and for OXPHOS complex stability and assembly into supercomplexes. ..
  4. Bacman S, Kauppila J, Pereira C, Nissanka N, Miranda M, Pinto M, et al. MitoTALEN reduces mutant mtDNA load and restores tRNAAla levels in a mouse model of heteroplasmic mtDNA mutation. Nat Med. 2018;24:1696-1700 pubmed publisher
    ..The molecular defect, namely a decrease in transfer RNAAla levels, was restored by the treatment. These results showed that mitoTALENs, when expressed in affected tissues, could revert disease-related phenotypes in mice. ..
  5. Pinto M, Vempati U, Diaz F, Peralta S, Moraes C. Ablation of Cytochrome c in Adult Forebrain Neurons Impairs Oxidative Phosphorylation Without Detectable Apoptosis. Mol Neurobiol. 2019;56:3722-3735 pubmed publisher
  6. Nissanka N, Bacman S, Plastini M, Moraes C. The mitochondrial DNA polymerase gamma degrades linear DNA fragments precluding the formation of deletions. Nat Commun. 2018;9:2491 pubmed publisher
  7. Pereira C, Bacman S, Arguello T, Zekonyte U, Williams S, Edgell D, et al. mitoTev-TALE: a monomeric DNA editing enzyme to reduce mutant mitochondrial DNA levels. EMBO Mol Med. 2018;10: pubmed publisher
    ..mitoTev-TALE provides an effective architecture for mtDNA editing that could facilitate therapeutic delivery of mtDNA editing enzymes to affected tissues. ..
  8. Bacman S, Williams S, Pinto M, Moraes C. The use of mitochondria-targeted endonucleases to manipulate mtDNA. Methods Enzymol. 2014;547:373-97 pubmed publisher
    ..This chapter describes the techniques and approaches used to test these designer enzymes. ..
  9. Pinto M, Moraes C. Mechanisms linking mtDNA damage and aging. Free Radic Biol Med. 2015;85:250-8 pubmed publisher
    ..Here, we review the changes that mtDNA undergoes during aging and the past and most recent hypotheses linking these changes to the tissue failure observed in aging. ..

More Information


  1. Moraes C, Kenyon L, Hao H. Mechanisms of human mitochondrial DNA maintenance: the determining role of primary sequence and length over function. Mol Biol Cell. 1999;10:3345-56 pubmed
    ..In agreement with this hypothesis, marked variations in mtDNA levels did not affect the transcription of nuclear-coded factors involved in mtDNA replication. ..
  2. Peralta S, Goffart S, Williams S, Diaz F, Garcia S, Nissanka N, et al. ATAD3 controls mitochondrial cristae structure in mouse muscle, influencing mtDNA replication and cholesterol levels. J Cell Sci. 2018;131: pubmed publisher
    ..i>This article has an associated First Person interview with the first author of the paper. ..
  3. request reprint
    Pereira C, Moraes C. Current strategies towards therapeutic manipulation of mtDNA heteroplasmy. Front Biosci (Landmark Ed). 2017;22:991-1010 pubmed
    ..The current strategies to induce heteroplasmy shift of mtDNA and its implications will be comprehensively discussed. ..
  4. Tengan C, Moraes C. NO control of mitochondrial function in normal and transformed cells. Biochim Biophys Acta Bioenerg. 2017;1858:573-581 pubmed publisher
    ..This article is part of a Special Issue entitled Mitochondria in Cancer, edited by Giuseppe Gasparre, Rodrigue Rossignol and Pierre Sonveaux. ..
  5. Pinto M, Nissanka N, Peralta S, Brambilla R, Diaz F, Moraes C. Pioglitazone ameliorates the phenotype of a novel Parkinson's disease mouse model by reducing neuroinflammation. Mol Neurodegener. 2016;11:25 pubmed publisher
    ..The motor phenotypes were improved by Pioglitazone treatment, suggesting that targetable secondary pathways can influence the development of certain forms of PD. ..
  6. Peralta S, Garcia S, Yin H, Arguello T, Diaz F, Moraes C. Sustained AMPK activation improves muscle function in a mitochondrial myopathy mouse model by promoting muscle fiber regeneration. Hum Mol Genet. 2016;25:3178-3191 pubmed publisher
    ..We conclude that although increase in mitochondrial biogenesis and other pathways may contribute, the main mechanism by which AICAR improves the myopathy phenotype is by promoting muscle regeneration. ..
  7. Gammage P, Moraes C, Minczuk M. Mitochondrial Genome Engineering: The Revolution May Not Be CRISPR-Ized. Trends Genet. 2018;34:101-110 pubmed publisher
    ..However, the existence of an endogenous mechanism for nucleic acid import into mammalian mitochondria, a prerequisite for mitochondrial CRISPR/Cas9 gene editing, remains controversial. ..
  8. Vempati U, Diaz F, Barrientos A, Narisawa S, Mian A, Millan J, et al. Role of cytochrome C in apoptosis: increased sensitivity to tumor necrosis factor alpha is associated with respiratory defects but not with lack of cytochrome C release. Mol Cell Biol. 2007;27:1771-83 pubmed
    ..These studies underscore the importance of oxidative phosphorylation and apoptosome function to both the intrinsic and extrinsic apoptotic pathways. ..