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Int Rev Cell Mol Biol. 2018;340:209-344. doi: 10.1016/bs.ircmb.2018.05.006. Epub 2018 Jun 22.

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

Author information

1
Department of Morphology Surgery and Experimental Medicine, Section of Pathology Oncology and Experimental Biology, Interdisciplinary Center for the Study of Inflammation (ICSI), Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy.
2
Department of Biochemistry, Nencki Institute of Experimental Biology, Polish Academy of Sciences, Warsaw, Poland.
3
Department of Cell and Developmental Biology, Consortium for Mitochondrial Research, University College London, London, United Kingdom.
4
Department of Morphology Surgery and Experimental Medicine, Section of Pathology Oncology and Experimental Biology, Interdisciplinary Center for the Study of Inflammation (ICSI), Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy; Cecilia Hospital, GVM Care & Research, 48033 Cotignola, Ravenna, Italy; Maria Pia Hospital, GVM Care & Research, Torino, Italy.
5
Institute of Molecular Toxicology and Pharmacology, Helmholtz Center Munich, German Research Center for Environmental Health, Neuherberg, Germany.
6
Department of Molecular Biology, University of Gdańsk, Gdańsk, Poland.
7
Department of Medicine, Division of Gastroenterology and Liver Diseases, Marion Bessin Liver Research Center, Albert Einstein College of Medicine, Bronx, NY, United States.
8
Clinica Medica "A. Murri", Dept. of Biomedical Sciences & Human Oncology, University of Bari "Aldo Moro" Medical School, Bari, Italy.
9
Institute of Molecular Toxicology and Pharmacology, Helmholtz Center Munich, German Research Center for Environmental Health, Neuherberg, Germany; Institute of Toxicology and Environmental Hygiene, Technical University Munich, Munich, Germany.
10
Departments of Cell Biology and Gottesman Institute for Stem Cell & Regenerative Medicine Research, Albert Einstein College of Medicine, Bronx, NY, United States.
11
Department of Pathology, The Children's Memorial Health Institute, Warsaw, Poland.
12
The Francis Crick Institute, London, United Kingdom.
13
Department of Cell and Developmental Biology, Consortium for Mitochondrial Research, University College London, London, United Kingdom; The Francis Crick Institute, London, United Kingdom; Department of Biomedical Sciences, University of Padua, Padua, Italy.
14
Cecilia Hospital, GVM Care & Research, 48033 Cotignola, Ravenna, Italy; Department of Biomedical Sciences, University of Padua, Padua, Italy.
15
CNC - Center for Neuroscience and Cell Biology, UC-Biotech, Biocant Park, University of Coimbra, Cantanhede, Portugal.
16
Department of Morphology Surgery and Experimental Medicine, Section of Pathology Oncology and Experimental Biology, Interdisciplinary Center for the Study of Inflammation (ICSI), Laboratory for Technologies of Advanced Therapies (LTTA), University of Ferrara, Ferrara, Italy; Cecilia Hospital, GVM Care & Research, 48033 Cotignola, Ravenna, Italy.

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.

KEYWORDS:

Age-related neurodegenerative disorders; Aging; Anti-ROS intervention; Antioxidant defense; Mitochondria; Mitochondrial dysfunction–related pathologies; ROS

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