Journal article
Chemotherapeutic-Induced Cardiovascular Dysfunction: Physiological Effects, Early Detection-The Role of Telomerase to Counteract Mitochondrial Defects and Oxidative Stress
International journal of molecular sciences, Vol.19(3), p.797
03/01/2018
DOI: 10.3390/ijms19030797
PMCID: PMC5877658
PMID: 29534446
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.
Details
- Title: Subtitle
- Chemotherapeutic-Induced Cardiovascular Dysfunction: Physiological Effects, Early Detection-The Role of Telomerase to Counteract Mitochondrial Defects and Oxidative Stress
- Creators
- Nabeel Quryshi - Medical College of WisconsinLaura E Norwood Toro - Medical College of WisconsinKarima Ait-Aissa - Medical College of WisconsinAmanda Kong - Medical College of WisconsinAndreas M. Beyer - Medical College of Wisconsin
- Resource Type
- Journal article
- Publication Details
- International journal of molecular sciences, Vol.19(3), p.797
- DOI
- 10.3390/ijms19030797
- PMID
- 29534446
- PMCID
- PMC5877658
- NLM abbreviation
- Int J Mol Sci
- ISSN
- 1661-6596
- eISSN
- 1422-0067
- Publisher
- Mdpi
- Number of pages
- 32
- Grant note
- Advancing a Healthier Wisconsin Endowment through MCW Redox Biology program MCWs We Care Fund for Medical Innovation and Research R01 HL133029 / NIH; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA 16POST26430075 / AHA; American Heart Association R01HL133029 / NATIONAL HEART, LUNG, AND BLOOD INSTITUTE; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Heart Lung & Blood Institute (NHLBI)
- Language
- English
- Date published
- 03/01/2018
- Academic Unit
- Cardiovascular Medicine; Internal Medicine
- Record Identifier
- 9984359926702771
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