Aging, Mitochondria, and Antioxidants

Dear Colleagues,

The elderly population is continually increasing worldwide due to increased life expectancy. The major challenge for elders is an increased occurrence of heart failure due to augmented cell injury in response to superimposed acute cardiac diseases, including acute myocardial infarction, increases in left ventricular afterload due to aortic stenosis or hypertension, chemotherapeutic agent cardiotoxicity, catecholamine-induced stress, or cardiac ischemia secondary to exogenous cardiac disease such as sepsis. Elderly patients sustain larger infarcts with greater mortality following the acute ischemia–reperfusion of acute coronary syndromes and their treatment. Increased cardiac injury with advanced age has also been shown in animal models. Many studies show that mitochondrial dysfunction has a pivotal role in the increased susceptibility to cellular injury in the aging heart. Although mitochondria are critical to maintaining normal cardiac function because they provide a constant energy supply and support metabolic homeostasis, dysfunctional mitochondria are key sources of cardiac injury in pathologic settings. Damaged mitochondria not only decrease energy supply, but also increase the generation of reactive oxygen species (ROS) and favor the opening of the mitochondrial permeability transition pore that contributes to cardiac injury. The mitochondrial electron transport chain (ETC) is a key site of ROS generation. Many studies show that aging impairs the ETC in a manner that increases ROS generation. ROS production is also regulated by a system of antioxidant enzymes. Aging also potentially leads to decreased antioxidant capability in cardiac mitochondria. Thus, oxidative stress during aging can be due to increased ROS generation from dysfunctional mitochondria or decreased antioxidant effect—especially antioxidant enzymes located within the mitochondria. Interestingly, recent studies show that age-induced mitochondrial defects in the ETC can be improved. Treatments including the supplementation of metformin, 4-PBA, and SS-31 can improve mitochondrial function in aged heart mitochondria. The effects of these treatments on antioxidants in aged heart mitochondria need to be studied further. We anticipate that more treatment options can be used to improve aging-induced mitochondrial dysfunction.

In this Special Issue, we invite original research articles on research linked to potential strategies targeted to improve mitochondrial function in aged hearts, especially by decreasing ROS generation or increasing antioxidant function, especially in the alteration of PRDXs, GRX2, and p66shc. All manuscripts should be submitted online. 

Dr. Edward Lesnefsky
Dr. Qun Chen
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

• aging
• mitochondrial respiratory chain
• antioxidants
• reactive oxygen species