A Mitochondrial Paradigm of Metabolic and Degenerative Diseases, Aging, and Cancer: A Dawn for Evolutionary Medicine

By Douglas C. Wallace. Annual Review of Genetics, 2005

3,308 citations recorded by the source corpus.

Subfields: Clinical Biochemistry, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/16399f848bb04faabd7f0107459132cc1c4777b0

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Citations in the corpus

Sirtuin Regulation of Mitochondria - Energy Production, Apoptosis, and Signaling (2010, background): “Mitochondria play critical roles in energy production, metabolism, apoptosis, and intracellular signaling [1-3].”
The pathways of mitophagy for quality control and clearance of mitochondria (2012, background): “Reactive oxygen species (ROS), in particular superoxide anion (O2 ), hydrogen peroxide (H2O2), and hydroxyl radical ( OH) are toxic byproducts of oxidative phosphorylation.(2) ROS causes oxidative damage to mitochondrial lipids, DNA, and proteins, making mitochondria”
Nitric oxide‐induced mitochondrial fission is regulated by dynamin‐related GTPases in neurons (2006, background): “To accommodate high-energy demands a single neuron harbors several hundreds of mitochondria (BereiterHahn and Voth, 1994; Wallace, 2005) that are dynamic, able to migrate, fuse and divide.”
SIRT1 is required for AMPK activation and the beneficial effects of resveratrol on mitochondrial function (2012, background): “…mitochondrial function in normal individuals may underlie a number of common age-related diseases (de Moura et al., 2010; Figueiredo et al., 2009; Wallace, 2005) and that treatments that stimulate mitochondrial function can delay the progression of some of these diseases (Baur et al., 2006;…”
A mitochondrial protein compendium elucidates complex I disease biology (2008, positive): “Mitochondrial dysfunction causes over 50 diseases ranging from neonatal fatalities to adult-onset neurodegeneration and is a likely contributor to 112 Cell 134, 112–123, July 11, 2008 ª2008 Elsevier Inc. cancer and type II diabetes (DiMauro and Schon, 2003; Lowell and Shulman, 2005; Wallace, 2005).”
p62/SQSTM1 is required for Parkin-induced mitochondrial clustering but not mitophagy; VDAC1 is dispensable for both (2010, background): “As mitochondrial damage accumulates with age, particularly in post-mitotic cells with high metabolic demands and/or high oxidation stress, mitochondria can become impaired thereby decreasing energy output, increasing ROS production and diminishing calcium-buffering capacity.(1) Increased ROS product”
Atg32 is a mitochondrial protein that confers selectivity during mitophagy (2009, background): “The accumulation of damaged protein and DNA in mitochondria is related to aging, cancer and neurodegenerative diseases (Wallace, 2005).”
Sirt3 Mediates Reduction of Oxidative Damage and Prevention of Age-related Hearing Loss under Caloric Restriction (2010, background): “Consistent with this hypothesis, mitochondria are a major source of ROS and of ROS-induced oxidative damage, and mitochondrial function declines during aging (Wallace, 2005).”
Metabolic control of mitochondrial biogenesis through the PGC-1 family regulatory network (2010, background): “through the bi-directional synthesis of multigenic transcripts, followed by the processing, polyadenylation and translation of individual mRNAs [4,5].”
Energetic Competition Between Neandertals and Anatomically Modern Humans (2009, background): “ences in thermogenesis and brown fat metabolism existed between Neandertal and modern humans (see Steegman et al. 2002; Wallace 2005), which may have given modern humans a physiological adaptation to cold that was effective in the context of less-massive body size.”