Journal article
Mitochondria as a Source and Target of Lipid Peroxidation Products in Healthy and Diseased Heart
Clinical and experimental pharmacology & physiology, Vol.39(2), pp.179-193
02/2012
DOI: 10.1111/j.1440-1681.2011.05641.x
PMCID: PMC3827773
PMID: 22066679
Abstract
The heart is a highly oxidative organ in which cardiomyocyte turnover is virtually absent, making it particularly vulnerable to accumulation of lipid peroxidation products (LPPs) formed as a result of oxidative damage.
Reactive oxygen and nitrogen species are the most common electrophiles formed during lipid peroxidation and lead to the formation of both stable and unstable lipid peroxidation products (LPPs). Of the LPPs formed, highly reactive aldehydes are a well-recognized causative factor in aging and age-associated diseases including cardiovascular disease and diabetes.
Recent studies have identified that the mitochondria are both a primary source and target of LPPs, with specific emphasis on aldehydes in cardiomyocytes, and how these affect the electron transport system and Ca
2+
balance.
A number of studies have found that there are functional consequences in the heart as a consequence of exposure to specific aldehydes (acrolein, trans-2-hexanal, 4-hydroxynonenal, and acetaldehyde). Since these LPPs are known to form in heart failure, cardiac ischemia/reperfusion injury, and diabetes, they may have an underappreciated role in the pathophysiology of these disease processes.
LPPs are involved in transcriptionally regulating endogenous anti-oxidant systems. Recent evidence has demonstrated that transient increases in LPPs might be beneficial in cardioprotection by contributing to mito-hormesis (i.e. this induction of anti-oxidant systems) in cardiomyocytes. Thus, exploitation of cardioprotective actions of LPPs may represent a novel therapeutic strategy for future treatment of heart disease.
Details
- Title: Subtitle
- Mitochondria as a Source and Target of Lipid Peroxidation Products in Healthy and Diseased Heart
- Creators
- Ethan J Anderson - Department of Pharmacology & Toxicology, East Carolina UniversityLalage A Katunga - Department of Pharmacology & Toxicology, East Carolina UniversityMonte S Willis - Department of Pathology, University of North Carolina at Chapel Hill
- Resource Type
- Journal article
- Publication Details
- Clinical and experimental pharmacology & physiology, Vol.39(2), pp.179-193
- DOI
- 10.1111/j.1440-1681.2011.05641.x
- PMID
- 22066679
- PMCID
- PMC3827773
- NLM abbreviation
- Clin Exp Pharmacol Physiol
- ISSN
- 0305-1870
- eISSN
- 1440-1681
- Grant note
- R21 HL098780 || HL / National Heart, Lung, and Blood Institute : NHLBI
- Language
- English
- Date published
- 02/2012
- Academic Unit
- Pharmaceutical Sciences and Experimental Therapeutics; Fraternal Order of Eagles Diabetes Research Center; Health, Sport, and Human Physiology
- Record Identifier
- 9984065316502771
Metrics
22 Record Views