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Open AccessJournal ArticleDOI

The Maintenance of Mitochondrial DNA Integrity—Critical Analysis and Update

TLDR
This review attempts to present a unified view of the current understanding of the process of DNA repair in mitochondria with an emphasis on issues that appear controversial.
Abstract
DNA molecules in mitochondria, just like those in the nucleus of eukaryotic cells, are constantly damaged by noxious agents. Eukaryotic cells have developed efficient mechanisms to deal with this assault. The process of DNA repair in mitochondria, initially believed nonexistent, has now evolved into a mature area of research. In recent years, it has become increasingly appreciated that mitochondria possess many of the same DNA repair pathways that the nucleus does. Moreover, a unique pathway that is enabled by high redundancy of the mitochondrial DNA and allows for the disposal of damaged DNA molecules operates in this organelle. In this review, we attempt to present a unified view of our current understanding of the process of DNA repair in mitochondria with an emphasis on issues that appear controversial.

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Journal ArticleDOI

Mitochondrial ROS in cancer: initiators, amplifiers or an Achilles' heel?

TL;DR: The targeted disruption of mitochondria-to-cell redox communication represents a promising avenue for future therapy for cancer treatment.
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Mitochondria-Targeted Triphenylphosphonium-Based Compounds: Syntheses, Mechanisms of Action, and Therapeutic and Diagnostic Applications

TL;DR: The physicochemical basis for mitochondrial accumulation of lipophilic cations, synthetic chemistry strategies to target compounds to mitochondria, mitochondrial probes, and sensors, and examples of mitochondrial targeting of bioactive compounds are described.
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Base excision repair: a critical player in many games.

TL;DR: This perspective reviews the many dimensions of base excision repair from a 10,000 foot vantage point and provides one person's view on where the field is headed and outlines the many base excison repair-related mysteries that have yet to be unraveled.
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CHK2 kinase in the DNA damage response and beyond

TL;DR: The activity of CHK2 in response to DNA damage and in the maintenance of the biological functions in unstressed cells are discussed and their activities are considered in relation to a possible role of CHk2 in tumorigenesis and, as a consequence, in the target of cancer therapy.
Journal ArticleDOI

Nuclear DNA damage signalling to mitochondria in ageing

TL;DR: Pharmacological modulation of NM signalling is a promising novel approach for the prevention and treatment of age-associated diseases.
References
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Journal ArticleDOI

How mitochondria produce reactive oxygen species.

TL;DR: The description outlined here facilitates the understanding of factors that favour mitochondrial ROS production and develops better methods to measure mitochondrial O2•− and H2O2 formation in vivo, as uncertainty about these values hampers studies on the role of mitochondrial ROS in pathological oxidative damage and redox signalling.
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Instability and decay of the primary structure of DNA

TL;DR: The spontaneous decay of DNA is likely to be a major factor in mutagenesis, carcinogenesis and ageing, and also sets limits for the recovery of DNA fragments from fossils.
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Rapid evolution of animal mitochondrial DNA.

TL;DR: The rate of evolution of the mitochondrial genome appears to exceed that of the single-copy fraction of the nuclear genome by a factor of about 10 and is likely to be an extremely useful molecule to employ for high-resolution analysis of the evolutionary process.
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A Mitochondrial Paradigm of Metabolic and Degenerative Diseases, Aging, and Cancer: A Dawn for Evolutionary Medicine

TL;DR: The mitochondria provide a direct link between the authors' environment and their genes and the mtDNA variants that permitted their forbears to energetically adapt to their ancestral homes are influencing their health today.
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Mitochondrial DNA mutation associated with Leber's hereditary optic neuropathy

TL;DR: This finding demonstrated that a nucleotide change in a mitochondrial DNA energy production gene can result in a neurological disease.
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