Mitochondria, oxidants, and aging.

By R. Balaban, S. Nemoto, Toren Finkel. Cell, 2005

4,313 citations recorded by the source corpus.

Subfields: Aging, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/57047b3d8094ae70b9eed8c4019c87ac8171ad59

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Citations in the corpus

Calorie restriction reduces oxidative stress by SIRT3-mediated SOD2 activation. (2010, background): “Since 90% of cellular ROS are produced in the mitochondria (Balaban et al., 2005), we set out to investigate whether SIRT3, a mammalian SIR2 homolog localized in the mitochondria (Onyango et al., 2002; Schwer et al., 2002), mediates the CR response and reduces oxidative stress.”
Sirt3 Mediates Reduction of Oxidative Damage and Prevention of Age-related Hearing Loss under Caloric Restriction (2010, background): “The mitochondrial free radical theory of aging postulates that aging results from accumulated oxidative damage caused by reactive oxygen species (ROS), originating from the mitochondrial respiratory chain (Balaban et al., 2005).”
Amyloid β-based therapy for Alzheimer’s disease: challenges, successes and future (2023, background): “Instead, most proteins of the mitochondria are synthesized by cytosolic ribosomes then imported into the organelle.202 APP- or Aβ-induced impairment of mitochondrial import pathway has been considered as a hallmark of AD.203–205 It has been demonstrated that APP blocked mitochondrial import machiner”
MICU1 is an Essential Gatekeeper for MCU-Mediated Mitochondrial Ca2+ Uptake That Regulates Cell Survival (2012, positive): “Physiological mROS is implicated in many processes including gene expression, cell growth, proliferation and differentiation, whereas excessive mROS promotes cell death (Balaban et al., 2005; Hamanaka and Chandel, 2010).”
From estrogen-centric to aging and oxidative stress: a revised perspective of the pathogenesis of osteoporosis. (2010, background): “To date, more than 50 yr since it was proposed by Harman (42), the most enduring theory of aging stipulates that OS resulting from an increase in intracellular ROS is the major determinant of aging and lifespan (43–45), as well as the culprit in several degenerative disorders associated with aging (”
Studies on free radicals, antioxidants, and co-factors (2007, background): “Many theories have been put forward to explain the phenomenon of aging (Armbrecht 2001; Biesalski 2002; Finkel and Holbrook 2002; Sohal et al 2002; Balaban et al 2005); and all of these have their strengths and weaknesses, and it’s likely that they all contribute to the mechanisms of aging.”
Disorders of bone remodeling. (2011, background): “Reactive oxygen species (ROS), the radical forms of oxygen, are produced in the mitochondria as by-products of respiration and oxidase activity and in cellular responses to various external stimuli ranging from inflammatory cytokines to ionizing radiation (88).”
Akt determines replicative senescence and oxidative or oncogenic premature senescence and sensitizes cells to oxidative apoptosis (2008, background): “Multiple experiments have shown that ROS play a critical role in determining life span and cellular senescence in mammalian cells (reviewed in Balaban et al., 2005).”
Mitochondrial reactive oxygen species promote production of proinflammatory cytokines and are elevated in TNFR1-associated periodic syndrome (TRAPS) (2011, background): “These results identify mitochondria, which are a major source of physiological cellular ROS (Chance et al., 1979; Balaban et al., 2005), in the genesis of ROS that drive inflammation.”