Oxidative Stress, Mitochondrial Dysfunction, and Aging
By Hang Cui, Yahui Kong, Hong Zhang. Journal of signal transduction, 2011
983 citations recorded by the source corpus.
Aging is an intricate phenomenon characterized by progressive decline in physiological functions and increase in mortality that is often accompanied by many pathological diseases. Although aging is almost universally conserved among all organisms, the underlying molecular mechanisms of aging remain largely elusive. Many theories of aging have been proposed, including the free-radical and mitochondrial theories of aging. Both theories speculate that cumulative damage to mitochondria and mitochondrial DNA (mtDNA) caused by reactive oxygen species (ROS) is one of the causes of aging. Oxidative damage affects replication and transcription of mtDNA and results in a decline in mitochondrial function which in turn leads to enhanced ROS production and further damage to mtDNA. In this paper, we will present the current understanding of the interplay between ROS and mitochondria and will discuss their potential impact on aging and age-related diseases.
Subfields: Aging, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/5fd7016cb70d2ca4fe7aa898e316a8d5abc4fdaa
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In Molecular Biology
Citations in the corpus
- The Role of the Reactive Oxygen Species and Oxidative Stress in the Pathomechanism of the Age-Related Ocular Diseases and Other Pathologies of the Anterior and Posterior Eye Segments in Adults (2016, background): “ROS can be generated at elevated rates under normal aging, as well as in acute or chronic pathophysiological conditions [4–6].”