Mitochondrial DNA Mutations, Oxidative Stress, and Apoptosis in Mammalian Aging

By G. Kujoth, A. Hiona, T. D. Pugh, Shinichi Someya, K. Panzer, S. Wohlgemuth, T. Hofer, Arnold Y. Seo, R. Sullivan, Wendy A. Jobling and 8 more. Science, 2005

2,111 citations recorded by the source corpus.

Subfields: Aging, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e13ea2d00f12a018fce44c7d11b4557c86e64040

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Citations in the corpus

Unravelling the Biological Roles of Reactive Oxygen Species (2011, background): “…experimental support for this link is weak as there are many examples of mouse models with severe respiratory chain dysfunction that do not have any major increase in hydrogen peroxide or superoxide production or oxidative damage (Wang et al., 2001; Trifunovic et al., 2005; Kujoth et al., 2005).”
Mitochondrial fusion is required for mtDNA stability in skeletal muscle and tolerance of mtDNA mutations (2010, neutral): “, 2007), PolgAD257A mutant (Kujoth et al., 2005), MLC-Cre (Bothe et al.”
The Mitochondrial Basis of Aging (2016, background): “One clear connection between mitochondria and stem cell function has come from the analysis of the previously described mtDNA mutator mice (Kujoth et al., 2005; Trifunovic et al., 2004).”
Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, positive): “Transgenic mice expressing a proofreading-deﬁcient version of the mtDNA polymerase g (POLG) accumulate mtDNA mutations and display features of premature ageing (Trifunovic et al , 2004; Kujoth et al , 2005).”
Mitochondrial dynamics in health and disease: mechanisms and potential targets (2023, background): “139,140 143 In yeast and C. elegans , downregulation of mitochondrial autophagy proteins results in mitochondrial damage and a shortening of lifespan.”
The role of mitochondria in aging. (2013, positive): “The mtDNA mutator mice have little or no increase in levels of ROS production and oxidative damage even though oxidative phosphorylation capacity is severely affected (59, 66).”
Mitochondrial rhomboid PARL regulates cytochrome c release during apoptosis via OPA1-dependent cristae remodeling. (2006, background): “in the Regulation of Apoptosis In the last few years, several intramembrane cleaving proteases have been identified, overturning the dogma that proteolysis(ahydrolyzingreaction)occursonlyinaqueous environments (Annaert and De Strooper, 2002; Brown et al., 2000; Freeman, 2004; Kopan and Ilagan, 2004”
Mitochondrial mutations in cancer (2006, background): “Within post-mitotic cells somatic mtDNA mutations accumulate over time, eroding cellular function (Trifunovic et al., 2004; Kujoth et al., 2005; Schriner et al., 2005).”