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HomeCirculation ResearchVol. 129, No. 5In This Issue Free AccessIn BriefPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessIn BriefPDF/EPUBIn This Issue Ruth Williams Ruth WilliamsRuth Williams Search for more papers by this author Originally published19 Aug 2021https://doi.org/10.1161/RES.0000000000000499Circulation Research. 2021;129:511is related toElectronic and Tobacco Cigarettes Alter Polyunsaturated Fatty Acids and Oxidative Biomarkersis related toGlucose Derivative Induced Vasculopathy in Children on Chronic Peritoneal DialysisSilencing Myeloid Netrin-1 Induces Inflammation Resolution and Plaque RegressionElectronic and Tobacco Cigarettes Alter Polyunsaturated Fatty Acids and Oxidative Biomarkers (p 514)Gupta et al measure oxidized lipid biomarkers to assess health risks of electronic cigarettes.E-cigarettes have surged in popularity in the last decade. While they are generally viewed as a safe alternative to smoking tobacco, studies suggest that E-cigarettes, like tobacco ones, cause oxidative stress, inflammation and endothelial dysfunction in users. Indeed, the aerosols produced during vaping contain comparable levels of reactive oxygen species (ROS) to those in tobacco smoke. Data on the extent to which E-cigarette ROS influence cardiovascular health is lacking, however. To address this, Gupta and colleagues recruited 32 chronic users of E-cigarettes, 29 chronic tobacco smokers, and 45 individuals that used neither, and measured their plasma levels of oxidative biomarkers. The team found similarities and differences between E-cigarette and tobacco users. Both, for example, had increased plasma antioxidant capacity and decreased levels of oxidized linoleic acid compared with the levels seen in non-users, while arachidonic acid levels were raised in tobacco smokers and reduced in the E-cigarette users. Overall, however, biomarker levels were deemed to be intermediate for E-cigarette users between non-users and tobacco users. The study suggests, therefore, that while E-cigarettes carry a lower health risk than tobacco ones, they are by no means safe.Download figureDownload PowerPointGlucose Derivative Induced Vasculopathy in Children on Chronic Peritoneal Dialysis (p e102)Glucose degradation products damage blood vessels during dialysis, report Bartosova et al.Diabetes, high blood pressure and obesity are risk factors for both cardiovascular disease (CVD) and chronic kidney disease (CKD). Worse still, loss of kidney function and even dialysis itself are thought to exacerbate cardiovascular issues. In the case of dialysis, it’s thought that high levels of glucose degradation products (GDPs) in the dialysis fluids can promote the addition of sugar moieties to vascular proteins and lipids (glycation), causing vessel damage. To investigate this theory, Bartosova and colleagues studied vascular tissue from children with CKD receiving dialysis fluid with either high levels or low levels of GDPs, or that were not on dialysis at all. Proteome and transcriptome analyses of the vessel tissues revealed that, compared with patients on no or low-GDP fluids, patients receiving high-GDP fluids had higher levels of damaging glycation, increased transcription of genes involved in cell death, and decreased transcription of genes involved in cell survival and cytoskeleton organization. In line with these findings, vessels from high-GDP patients displayed considerable evidence of damage (apoptosis, cytoskeletal disintergration, thickened intimas). The results thus confirm GDPs can cause vasculopathy and suggest low-GDP fluids should be favored for dialysis.Download figureDownload PowerPointTargeting Netrin-1 in Established Atherosclerosis Promotes Inflammation Resolution and Plaque Regression (p 530)Blocking netrin-1 diminishes atherosclerotic plaques in mice, say Schlegel et al.While excess lipids in the blood spur the development of atherosclerosis, the disease quickly becomes one of chronic inflammation that encourages the persistence of the lipid-filled plaques in vessel walls. Indeed, sustained inflammation is thought to explain why lipid-lowering drugs often aren’t enough to combat the condition. Inflammation-suppressing drugs are also being investigated, but because these may cause susceptibility to infections, Schlegel and colleagues reasoned that promoting resolution of inflammation may be a preferable goal. To that end, the team tested blocking nectrin-1 in atherosclerosis-prone mice. Originally identified as a factor essential for nerve cells, Netrin-1 has also been found in macrophages where it promotes persistence and survival of the cells in atherosclerotic plaques. The team showed that in mice with advanced atherosclerosis, turning off netrin-1 in macrophages—via an inducible genetic switch—led to significant plaque regression. Not only did plaque macrophages exhibit reduced retention, proliferation and survival, those that remained were more likely to be pro-resolving. While susceptibility to infection was not investigated in this study, the results suggest in principle that netrin-1 blockade could be a strategy for atherosclerosis treatment.Download figureDownload PowerPoint Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesElectronic and Tobacco Cigarettes Alter Polyunsaturated Fatty Acids and Oxidative BiomarkersRajat Gupta, et al. Circulation Research. 2021;129:514-526Glucose Derivative Induced Vasculopathy in Children on Chronic Peritoneal DialysisMaria Bartosova, et al. Circulation Research. 2021;129:e102-e118Silencing Myeloid Netrin-1 Induces Inflammation Resolution and Plaque RegressionMartin Schlegel, et al. Circulation Research. 2021;129:530-546 August 20, 2021Vol 129, Issue 5 Advertisement Article InformationMetrics © 2021 American Heart Association, Inc.https://doi.org/10.1161/RES.0000000000000499 Originally publishedAugust 19, 2021 PDF download Advertisement