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Int. J. Mol. Sci. 2018, 19(3), 797; https://doi.org/10.3390/ijms19030797

Chemotherapeutic-Induced Cardiovascular Dysfunction: Physiological Effects, Early Detection—The Role of Telomerase to Counteract Mitochondrial Defects and Oxidative Stress

1
Department of Medicine, Medical College of Wisconsin, Milwaukee, WI 53226, USA
2
Department of Physiology, Cardiovascular Center and Redox Biology Program, Medical College of Wisconsin, Milwaukee, WI 53226, USA
3
Department of Surgery, Medical College of Wisconsin, Milwaukee, WI 53226, USA
*
Author to whom correspondence should be addressed.
Received: 5 January 2018 / Revised: 7 March 2018 / Accepted: 7 March 2018 / Published: 10 March 2018
(This article belongs to the Special Issue Role of Telomeres and Telomerase in Cancer and Aging)
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Abstract

Although chemotherapeutics can be highly effective at targeting malignancies, their ability to trigger cardiovascular morbidity is clinically significant. Chemotherapy can adversely affect cardiovascular physiology, resulting in the development of cardiomyopathy, heart failure and microvascular defects. Specifically, anthracyclines are known to cause an excessive buildup of free radical species and mitochondrial DNA damage (mtDNA) that can lead to oxidative stress-induced cardiovascular apoptosis. Therefore, oncologists and cardiologists maintain a network of communication when dealing with patients during treatment in order to treat and prevent chemotherapy-induced cardiovascular damage; however, there is a need to discover more accurate biomarkers and therapeutics to combat and predict the onset of cardiovascular side effects. Telomerase, originally discovered to promote cellular proliferation, has recently emerged as a potential mechanism to counteract mitochondrial defects and restore healthy mitochondrial vascular phenotypes. This review details mechanisms currently used to assess cardiovascular damage, such as C-reactive protein (CRP) and troponin levels, while also unearthing recently researched biomarkers, including circulating mtDNA, telomere length and telomerase activity. Further, we explore a potential role of telomerase in the mitigation of mitochondrial reactive oxygen species and maintenance of mtDNA integrity. Telomerase activity presents a promising indicator for the early detection and treatment of chemotherapy-derived cardiac damage. View Full-Text
Keywords: cardiac oncology; mtDNA damage; telomerase; telomerase activity; heart failure cardiac oncology; mtDNA damage; telomerase; telomerase activity; heart failure
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).
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Quryshi, N.; Norwood Toro, L.E.; Ait-Aissa, K.; Kong, A.; Beyer, A.M. Chemotherapeutic-Induced Cardiovascular Dysfunction: Physiological Effects, Early Detection—The Role of Telomerase to Counteract Mitochondrial Defects and Oxidative Stress. Int. J. Mol. Sci. 2018, 19, 797.

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