Extension of Murine Life Span by Overexpression of Catalase Targeted to Mitochondria

By S. Schriner, Nancy J. Linford, G. Martin, P. Treuting, C. Ogburn, M. Emond, P. Coskun, W. Ladiges, N. Wolf, H. Van Remmen and 2 more. Science, 2005

1,745 citations recorded by the source corpus.

Subfields: Aging, Biological Psychiatry, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/188014da02de31d388dfb83f40f31ea59f07095f

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Citations in the corpus

The Oxygen Rich Postnatal Environment Induces Cardiomyocyte Cell Cycle Arrest Through DNA Damage Response (2014, positive): “…catalase) mice, in which floxed transcriptional stop sequences are inserted in between universal GAPDH enhancer/promoter andmCAT (Dai et al., 2011; Schriner et al., 2005), with Myh6-Cre mice to generate mice expressing mCAT only in cardiomyocytes by cardiomyocyte-specific deletion of…”
The mitochondrial energy transduction system and the aging process. (2007, background): “(141) reported that transgenic mice that overexpressed human catalase in heart mitochondria have increased median and maximal life span.”
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).”
Reactive oxygen species act through p38 MAPK to limit the lifespan of hematopoietic stem cells (2006, background): “, it is controversial whether increasing antioxidative defenses enhances longevit”
Redox Regulation of Cell Survival (2008, positive): “These mice also exhibited a decrease in H2O2 level and in mtDNA damage (273).”
Mitochondria take center stage in aging and neurodegeneration (2005, background): “Recently it was shown, that overexpression of the antioxidant enzyme catalase, which converts H2O2 to H2O results in life span extension in long-lived mice.(15) The authors produced transgenic mice that overexpressed human catalase localized to the peroxisome, the nucleus, and the mitochondria.”
Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype (2015, background): “However, aging also entails loss of mitochondrial function (Schriner et al., 2005), and we showmany forms of mitochondrial dysfunction result in MiDAS.”
An integrated view of oxidative stress in aging: basic mechanisms, functional effects, and pathological considerations. (2007, background): “(237) showed that transgenic mice overexpressing human catalase in mitochondria had increases in both median and maximum life span by averages of 5 and 5.”
Mitochondrial Energetics and Therapeutics (2010, positive): “The resulting transgenic mice have an increased life span and reduced mtDNA somatic mutation rate, and they are also more resistant to oxidative challenge and to cardiomyopathy (262).”
A Mitochondrial Paradigm of Metabolic and Degenerative Diseases, Aging, and Cancer: A Dawn for Evolutionary Medicine (2005, background): “These protective effects to mitochondrial oxidation and mtDNA mutations were associated with a 21% increase in mean life span and a 10% increase in maximum life span in both male and female mitochondrial catalase transgenic animals (197).”
Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases (2006, positive): “However, it has recently been shown that overexpression of catalase experimentally targeted to mitochondria increased lifespan in an already long-lived mouse strai”