Aldrin V. Gomes

Namakkal S. Rajasekaran

Xinchun Pi

Oxidative Medicine and Cellular Longevity

PubMed

Gomes, Aldrin V

Rajasekaran, Namakkal S

Pi, Xinchun

eScholarship - University of California

UC DavisUC Davis Previously Published WorksTitleRedox Signaling and the Cardiovascular and Skeletal Muscle SystemPermalinkhttps://escholarship.org/uc/item/9qq5z6dkAuthorsGomes, Aldrin VRajasekaran, Namakkal SPi, XinchunPublication Date2015DOI10.1155/2015/849095 Peer reviewedeScholarship.org Powered by the California Digital LibraryUniversity of CaliforniaEditorialRedox Signaling and the Cardiovascular andSkeletal Muscle SystemAldrin V. Gomes,1 Namakkal S. Rajasekaran,2,3 and Xinchun Pi41Department of Neurobiology, Physiology, and Behavior, University of California, Davis, CA 95616, USA2Cardiac Aging & Redox Signaling Laboratory, Division of Molecular & Cellular Pathology, Department of Pathology,University of Alabama at Birmingham, Birmingham, AL 35294, USA3Division of Cardiovascular Medicine, Department of Medicine, University of Utah School of Medicine, Salt Lake City,UT 84132, USA4Department of Medicine, Cardiovascular Research Institute, Baylor College of Medicine, Houston, TX 77030, USACorrespondence should be addressed to Aldrin V. Gomes; avgomes@ucdavis.eduReceived 25 August 2015; Accepted 25 August 2015Copyright © 2015 Aldrin V. Gomes et al. This is an open access article distributed under the Creative Commons AttributionLicense, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properlycited.The role of reactive oxygen species (ROS) in skeletal, cardiac,and vascular dysfunctions has been under investigation fordecades. Over the last decade advanced in vitro and in vivoapproaches have significantly improved our understandingof the role of oxidative stress in cardiovascular and skeletalmuscle diseases. Oxidative stress is regarded as an imbalancebetween the production of free radicals/ROS and the cell’sintrinsic antioxidant defense mechanisms. Overburden ofoxidative stress has been associated with atherosclerosis,ischemic heart disease, hypertension, cardiomyopathies, car-diac hypertrophy, heart failure, and skeletal muscle diseasessuch asmuscular dystrophy and sarcopenia.This special issueprovides insights into understanding of the role of oxidativestress as a potential causal mechanism in various formsof cardiovascular and skeletal disease models and possibleprotection through antioxidant supplementation.The original research article by T. L. Lynch et al. demon-strates for the first time that oxidative stress is elevatedin a cardiac myosin binding protein C mouse model ofdilated cardiomyopathy (DCM). DCM heart homogenatesshow a lower reduced/oxidized glutathione (GSH/GSSG)ratio, increased oxidized (carbonylated) proteins, increasedlipid peroxidation, and reduced signals for mitochondrialsemiquinone radicals and Fe-S clusters (as measured byelectron paramagnetic resonance spectroscopy) comparedto healthy control heart homogenates. Similar results wereobtained when human cardiomyopathy heart homogenatesamples were investigated.These results strongly suggest thatoxidative stress may exacerbate the development of heartfailure.In the original study by L. A. Moreno-Ruı́z et. al., theauthors demonstrate the effects of oxidative stress on leftventricular mechanics in hypertensive patients. These stud-ies highlight the significance and contribution of oxidativestress in hypertensive patients with diastolic dysfunctionand preserved ejection fraction. Heart failure with preservedejection fraction is an emerging clinical condition in a widerange of cardiac patients that warrants further mechanisticunderstanding.The authors showed that a significant increasein the levels of oxidized proteins coupled with impairedantioxidant defenses in essential hypertensive patients mightbe a potential cause for cardiac dysfunction. The originalwork performed by A. Gawron-Skarbek et al. demonstratesan interesting observation that physically active and fit malepatients with coronary heart disease (CHD), whilst having amore favorable cardiometabolic diseases risk profile, are char-acterized by lowered antioxidant capacities. This manuscriptalso discovered that uric acid was not only a potentHindawi Publishing CorporationOxidative Medicine and Cellular LongevityVolume 2015, Article ID 849095, 2 pageshttp://dx.doi.org/10.1155/2015/8490952 Oxidative Medicine and Cellular Longevityantioxidant but also a cardiovascular risk factor.These resultsprovide insights for future planning of effective cardiacrehabilitation in CHD patients.The review by R. Ghosh et al. focuses on the role ofnonsteroidal anti-inflammatory drugs (NSAIDs) in cardio-vascular disease. NSAIDs are one of themost commonly useddrugs worldwide and have been associated with increasedrisk of cardiovascular disease. The authors present resultsto support their suggestion that the cardiovascular effectsmay be partly due to high ROS levels produced by NSAIDs.Another review by P. Angsutararux et al. outlined oxidativestress as a trigger/causative mechanism for chemotherapy-induced cardiotoxicity.The studies connecting chemotherapyand cardiotoxicity have attracted the field of cardiovascularresearch within the past decade. The authors elegantly out-lined the key published findings of the effects of different can-cer drugs that lead to structural and functional remodeling ofthe heart. Importantly, this review updates what is currentlyknown about the cross talk between chemotherapy, oxidativestress, and cardiotoxicity. ROS has been previously shown toaffect the function of oxygen sensing proteins. The review byW.H. D. Townley-Tilson et al. is focused on the crucial role ofoxygen sensing proteins in heart function and ischemic heartdisease. In particular, the review elaborates the recent excitingprogress about prolyl hydroxylase domain proteins (PHDs)in the regulation of cardiac homeostasis.Muscle wasting occurs due to aging or as consequence ofmany diseases including chronic kidney disease (CKD). Theoriginal research by D.-T. Wang et al. shows that CKD upreg-ulated the expression of myostatin and associated skeletalmuscle breakdown through activation of both autophagy andthe ubiquitin-proteasome system (UPS). These molecularevents are mechanistically linked to the PI3K/Akt/FoxO3asignaling pathway. The article by A. Felipe et al. shows con-vincing evidence from a group of 66 Chilean male volunteersindicating that serum levels of ferritin, a protein that regulatesiron homeostasis, are associated with metabolic syndromeand serve as a clinical or diagnostic marker for chronicdiseases that are related to oxidative stress, hepatic damage,insulin resistance, and renal insufficiency. Of interest, thisstudy identified a strong positive association between redmeat consumption and serum ferritin.Selenium (Se) is an exogenous antioxidant that performsits function by stimulating the expression of selenoproteinssuch as glutathione peroxidases (GPx) in endothelial cells.The original article by B. Ruseva et al. demonstrates thatSe supplementation increases GPx-1 activity and suppressedlipid peroxidation in rats. These results suggest that Se sup-plementation may be a potential therapeutic and preventivestrategy against vascular disease. The original article by J.-H.Shin et al. shows that ROS generated due to ischemia-reperfusion (I/R) injury in bladdermuscle reducemuscle ten-sion thereby increasing the risk of lower urinary tract symp-toms. The same study illustrated that the xanthine oxidaseinhibitor allopurinol could protect the rat urinary bladderfrom I/R injury and improved the contractile responses of themuscles in longitudinal bladder strips.All the articles in this special issue focus on redoxsignaling in the cardiovascular and skeletal muscle systemand provide a platform for the researchers to understandthe ROS based challenges in these pathologies. The topicscovered in this issue set the stage to addressmanyunansweredquestions in future.Aldrin V. GomesNamakkal S. RajasekaranXinchun Pi

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Redox Signaling and the Cardiovascular and Skeletal Muscle System

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EditorialRedox Signaling and the Cardiovascular andSkeletal Muscle SystemAldrin V. Gomes,1 Namakkal S. Rajasekaran,2,3 and Xinchun Pi41Department of Neurobiology, Physiology, and Behavior, University of California, Davis, CA 95616, USA2Cardiac Aging & Redox Signaling Laboratory, Division of Molecular & Cellular Pathology, Department of Pathology,University of Alabama at Birmingham, Birmingham, AL 35294, USA3Division of Cardiovascular Medicine, Department of Medicine, University of Utah School of Medicine, Salt Lake City,UT 84132, USA4Department of Medicine, Cardiovascular Research Institute, Baylor College of Medicine, Houston, TX 77030, USACorrespondence should be addressed to Aldrin V. Gomes; avgomes@ucdavis.eduReceived 25 August 2015; Accepted 25 August 2015Copyright © 2015 Aldrin V. Gomes et al. This is an open access article distributed under the Creative Commons AttributionLicense, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properlycited.The role of reactive oxygen species (ROS) in skeletal, cardiac,and vascular dysfunctions has been under investigation fordecades. Over the last decade advanced in vitro and in vivoapproaches have significantly improved our understandingof the role of oxidative stress in cardiovascular and skeletalmuscle diseases. Oxidative stress is regarded as an imbalancebetween the production of free radicals/ROS and the cell’sintrinsic antioxidant defense mechanisms. Overburden ofoxidative stress has been associated with atherosclerosis,ischemic heart disease, hypertension, cardiomyopathies, car-diac hypertrophy, heart failure, and skeletal muscle diseasessuch asmuscular dystrophy and sarcopenia.This special issueprovides insights into understanding of the role of oxidativestress as a potential causal mechanism in various formsof cardiovascular and skeletal disease models and possibleprotection through antioxidant supplementation.The original research article by T. L. Lynch et al. demon-strates for the first time that oxidative stress is elevatedin a cardiac myosin binding protein C mouse model ofdilated cardiomyopathy (DCM). DCM heart homogenatesshow a lower reduced/oxidized glutathione (GSH/GSSG)ratio, increased oxidized (carbonylated) proteins, increasedlipid peroxidation, and reduced signals for mitochondrialsemiquinone radicals and Fe-S clusters (as measured byelectron paramagnetic resonance spectroscopy) comparedto healthy control heart homogenates. Similar results wereobtained when human cardiomyopathy heart homogenatesamples were investigated.These results strongly suggest thatoxidative stress may exacerbate the development of heartfailure.In the original study by L. A. Moreno-Ruı´z et. al., theauthors demonstrate the effects of oxidative stress on leftventricular mechanics in hypertensive patients. These stud-ies highlight the significance and contribution of oxidativestress in hypertensive patients with diastolic dysfunctionand preserved ejection fraction. Heart failure with preservedejection fraction is an emerging clinical condition in a widerange of cardiac patients that warrants further mechanisticunderstanding.The authors showed that a significant increasein the levels of oxidized proteins coupled with impairedantioxidant defenses in essential hypertensive patients mightbe a potential cause for cardiac dysfunction. The originalwork performed by A. Gawron-Skarbek et al. demonstratesan interesting observation that physically active and fit malepatients with coronary heart disease (CHD), whilst having amore favorable cardiometabolic diseases risk profile, are char-acterized by lowered antioxidant capacities. This manuscriptalso discovered that uric acid was not only a potentHindawi Publishing CorporationOxidative Medicine and Cellular LongevityVolume 2015, Article ID 849095, 2 pageshttp://dx.doi.org/10.1155/2015/8490952 Oxidative Medicine and Cellular Longevityantioxidant but also a cardiovascular risk factor.These resultsprovide insights for future planning of effective cardiacrehabilitation in CHD patients.The review by R. Ghosh et al. focuses on the role ofnonsteroidal anti-inflammatory drugs (NSAIDs) in cardio-vascular disease. NSAIDs are one of themost commonly useddrugs worldwide and have been associated with increasedrisk of cardiovascular disease. The authors present resultsto support their suggestion that the cardiovascular effectsmay be partly due to high ROS levels produced by NSAIDs.Another review by P. Angsutararux et al. outlined oxidativestress as a trigger/causative mechanism for chemotherapy-induced cardiotoxicity.The studies connecting chemotherapyand cardiotoxicity have attracted the field of cardiovascularresearch within the past decade. The authors elegantly out-lined the key published findings of the effects of different can-cer drugs that lead to structural and functional remodeling ofthe heart. Importantly, this review updates what is currentlyknown about the cross talk between chemotherapy, oxidativestress, and cardiotoxicity. ROS has been previously shown toaffect the function of oxygen sensing proteins. The review byW.H. D. Townley-Tilson et al. is focused on the crucial role ofoxygen sensing proteins in heart function and ischemic heartdisease. In particular, the review elaborates the recent excitingprogress about prolyl hydroxylase domain proteins (PHDs)in the regulation of cardiac homeostasis.Muscle wasting occurs due to aging or as consequence ofmany diseases including chronic kidney disease (CKD). Theoriginal research by D.-T. Wang et al. shows that CKD upreg-ulated the expression of myostatin and associated skeletalmuscle breakdown through activation of both autophagy andthe ubiquitin-proteasome system (UPS). These molecularevents are mechanistically linked to the PI3K/Akt/FoxO3asignaling pathway. The article by A. Felipe et al. shows con-vincing evidence from a group of 66 Chilean male volunteersindicating that serum levels of ferritin, a protein that regulatesiron homeostasis, are associated with metabolic syndromeand serve as a clinical or diagnostic marker for chronicdiseases that are related to oxidative stress, hepatic damage,insulin resistance, and renal insufficiency. Of interest, thisstudy identified a strong positive association between redmeat consumption and serum ferritin.Selenium (Se) is an exogenous antioxidant that performsits function by stimulating the expression of selenoproteinssuch as glutathione peroxidases (GPx) in endothelial cells.The original article by B. Ruseva et al. demonstrates thatSe supplementation increases GPx-1 activity and suppressedlipid peroxidation in rats. These results suggest that Se sup-plementation may be a potential therapeutic and preventivestrategy against vascular disease. The original article by J.-H.Shin et al. shows that ROS generated due to ischemia-reperfusion (I/R) injury in bladdermuscle reducemuscle ten-sion thereby increasing the risk of lower urinary tract symp-toms. The same study illustrated that the xanthine oxidaseinhibitor allopurinol could protect the rat urinary bladderfrom I/R injury and improved the contractile responses of themuscles in longitudinal bladder strips.All the articles in this special issue focus on redoxsignaling in the cardiovascular and skeletal muscle systemand provide a platform for the researchers to understandthe ROS based challenges in these pathologies. The topicscovered in this issue set the stage to addressmanyunansweredquestions in future.Aldrin V. GomesNamakkal S. 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Redox Signaling and the Cardiovascular and Skeletal Muscle System

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