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Targeting Mitochondria to Counteract Age-Related Cellular Dysfunction

1
Molecular Biology and Biochemistry, Gottfried Schatz Research Center, Medical University of Graz; Neue Stiftingtalstraße 6/6, 8010 Graz, Austria
2
Department of Dentistry and Maxillofacial Surgery, Medical University of Graz; Billrothgasse 4, 8010 Graz, Austria
3
BioTechMed, Mozartgasse 12/2, 8010 Graz, Austria
*
Authors to whom correspondence should be addressed.
Genes 2018, 9(3), 165; https://doi.org/10.3390/genes9030165
Received: 10 January 2018 / Revised: 2 March 2018 / Accepted: 15 March 2018 / Published: 16 March 2018
(This article belongs to the Special Issue Mitochondria and Aging)
Senescence is related to the loss of cellular homeostasis and functions, which leads to a progressive decline in physiological ability and to aging-associated diseases. Since mitochondria are essential to energy supply, cell differentiation, cell cycle control, intracellular signaling and Ca2+ sequestration, fine-tuning mitochondrial activity appropriately, is a tightrope walk during aging. For instance, the mitochondrial oxidative phosphorylation (OXPHOS) ensures a supply of adenosine triphosphate (ATP), but is also the main source of potentially harmful levels of reactive oxygen species (ROS). Moreover, mitochondrial function is strongly linked to mitochondrial Ca2+ homeostasis and mitochondrial shape, which undergo various alterations during aging. Since mitochondria play such a critical role in an organism’s process of aging, they also offer promising targets for manipulation of senescent cellular functions. Accordingly, interventions delaying the onset of age-associated disorders involve the manipulation of mitochondrial function, including caloric restriction (CR) or exercise, as well as drugs, such as metformin, aspirin, and polyphenols. In this review, we discuss mitochondria’s role in and impact on cellular aging and their potential to serve as a target for therapeutic interventions against age-related cellular dysfunction. View Full-Text
Keywords: mitochondria; aging; caloric restriction; exercise; caloric restriction mimetics; polyphenols; aspirin mitochondria; aging; caloric restriction; exercise; caloric restriction mimetics; polyphenols; aspirin
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MDPI and ACS Style

Madreiter-Sokolowski, C.T.; Sokolowski, A.A.; Waldeck-Weiermair, M.; Malli, R.; Graier, W.F. Targeting Mitochondria to Counteract Age-Related Cellular Dysfunction. Genes 2018, 9, 165. https://doi.org/10.3390/genes9030165

AMA Style

Madreiter-Sokolowski CT, Sokolowski AA, Waldeck-Weiermair M, Malli R, Graier WF. Targeting Mitochondria to Counteract Age-Related Cellular Dysfunction. Genes. 2018; 9(3):165. https://doi.org/10.3390/genes9030165

Chicago/Turabian Style

Madreiter-Sokolowski, Corina T.; Sokolowski, Armin A.; Waldeck-Weiermair, Markus; Malli, Roland; Graier, Wolfgang F. 2018. "Targeting Mitochondria to Counteract Age-Related Cellular Dysfunction" Genes 9, no. 3: 165. https://doi.org/10.3390/genes9030165

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