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. 2019 May 11;8(2):32.
doi: 10.3390/biology8020032.

Drug-Induced Mitochondrial Toxicity in the Geriatric Population: Challenges and Future Directions

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Drug-Induced Mitochondrial Toxicity in the Geriatric Population: Challenges and Future Directions

Yvonne Will et al. Biology (Basel). .
Free PMC article


Mitochondrial function declines with age, leading to a variety of age-related diseases (metabolic, central nervous system-related, cancer, etc.) and medication usage increases with age due to the increase in diseases. Drug-induced mitochondrial toxicity has been described for many different drug classes and can lead to liver, muscle, kidney and central nervous system injury and, in rare cases, to death. Many of the most prescribed medications in the geriatric population carry mitochondrial liabilities. We have demonstrated that, over the past decade, each class of drugs that demonstrated mitochondrial toxicity contained drugs with both more and less adverse effects on mitochondria. As patient treatment is often essential, we suggest using medication(s) with the best safety profile and the avoidance of concurrent usage of multiple medications that carry mitochondrial liabilities. In addition, we also recommend lifestyle changes to further improve one's mitochondrial function, such as weight loss, exercise and nutrition.

Keywords: aging; drug-induced mitochondrial toxicity; polypharmacy.

Conflict of interest statement

The authors declare no conflict of interest.


Figure 1
Figure 1
Mitochondrial dysfunction is implicated in many age-related diseases such as metabolic diseases (T2DM, obesity, cardiovascular and cerebrovascular disease, Non-Alcoholic Fatty Liver Disease (NAFDL)) [2,3,4,5,6,7], CNS-related diseases (Parkinson’s, Alzheimer’s and Huntington’s disease, hearing loss, cataracts) [8,9,10,11], inflammation (osteoarthritis) [12], cancer [13,14], sarcopenia [15] and chronic obstructive pulmonary disease (COPD) [16].
Figure 2
Figure 2
Flow diagram illustrating the interrelationships governing mitochondrial homeostasis in response to the loss of mitochondrial function, such as that which occurs with aging. The Sirt1-dependent regulation of both PGC1α and AMPK provides a well-controlled integration of the disposal of dysfunctional mitochondria (mitophagy) and their replacement with new, supposedly fully functional, mitochondria (biogenesis).

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