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Mitochondria and Reactive Oxygen Species in Aging and Age-Related Diseases.

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TLDR
An update regarding the key roles of ROS-mitochondria cross talk in different fundamental physiological or pathological situations accompanying aging is provided, highlighting that mitochondrial ROS may be a decisive target in clinical practice.
Abstract
Aging has been linked to several degenerative processes that, through the accumulation of molecular and cellular damage, can progressively lead to cell dysfunction and organ failure. Human aging is linked with a higher risk for individuals to develop cancer, neurodegenerative, cardiovascular, and metabolic disorders. The understanding of the molecular basis of aging and associated diseases has been one major challenge of scientific research over the last decades. Mitochondria, the center of oxidative metabolism and principal site of reactive oxygen species (ROS) production, are crucial both in health and in pathogenesis of many diseases. Redox signaling is important for the modulation of cell functions and several studies indicate a dual role for ROS in cell physiology. In fact, high concentrations of ROS are pathogenic and can cause severe damage to cell and organelle membranes, DNA, and proteins. On the other hand, moderate amounts of ROS are essential for the maintenance of several biological processes, including gene expression. In this review, we provide an update regarding the key roles of ROS-mitochondria cross talk in different fundamental physiological or pathological situations accompanying aging and highlighting that mitochondrial ROS may be a decisive target in clinical practice.

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Reactive Oxygen Species: Drivers of Physiological and Pathological Processes

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References
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Journal ArticleDOI

Free Radicals in the Physiological Control of Cell Function

Wulf Dröge
TL;DR: There is growing evidence that aging involves, in addition, progressive changes in free radical-mediated regulatory processes that result in altered gene expression.
Journal ArticleDOI

Biochemistry and molecular cell biology of diabetic complications

TL;DR: This integrating paradigm provides a new conceptual framework for future research and drug discovery in diabetes-specific microvascular disease and seems to reflect a single hyperglycaemia-induced process of overproduction of superoxide by the mitochondrial electron-transport chain.
Journal ArticleDOI

Aging: A Theory Based on Free Radical and Radiation Chemistry

TL;DR: It seems possible that one factor in aging may be related to deleterious side attacks of free radicals (which are normally produced in the course of cellular metabolism) on cell constituents.
Journal ArticleDOI

Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium.

TL;DR: The multiple anginal episodes that often precede myocardial infarction in man may delay cell death after coronary occlusion, and thereby allow for greater salvage of myocardium through reperfusion therapy, which is proposed to protect the heart from a subsequent sustained ischemic insult.
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