HomeCirculation ResearchVol. 125, No. 8In 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 published26 Sep 2019https://doi.org/10.1161/RES.0000000000000301Circulation Research. 2019;125:725is related toReactive Vasodilation Predicts Mortality in Primary Systemic Light-Chain AmyloidosisMiro2 Regulates Inter-Mitochondrial Communication in the Heart and Protects Against TAC-Induced Cardiac DysfunctionCirculating Monocyte Chemoattractant Protein-1 and Risk of StrokeMiro2-Mediated Cardiac Mitochondrial Communication (p 728)Download figureDownload PowerPointIn the heart, Miro2 mediates mitochondrial communication and protects against hypertophy, say Cao et al.Heart cells have high energy demands and so require plenty of fully functioning mitochondria. To maintain mitochondrial health and performance, the organelles regularly communicate with each other. In many cells, this communication occurs via the fusion of mitochondria into giant networks, but in cardiomyocytes where mitochondrial movement is constrained, the organelles communicate by either kissing (a brief connection between neighboring mitochondria) or nanotunneling (a sustained connection by means of long nanometer-sized tubular protrusions called nanotubes). Cao and colleagues have now discovered a protein that controls this kissing and tunneling. Miro2 was identified as a mitochondrial transport protein, but in cardiomyocytes, the team found it associates with nanotubes, and its overexpression increases mitochondrial nanotunneling and kissing. In mice with hypertrophy, Miro2 expression was decreased, as was mitochondrial communication. Transgenic mice with increased Miro2 expression, by contrast, were more resistant to hypertrophy, maintaining better cardiac function than their wild-type counterparts. Together, the results reveal a novel role for Miro2 in mitochondrial communication and show that maintaining such communication may mitigate the effects of hypertrophy.Reactive Vasodilation in AL Amyloidosis (p 744)Download figureDownload PowerPointReactive vasodilation predicts mortality in light chain amyloidosis, report Stamatelopoulos et al.Light chain (AL) amyloidosis is a rare but deadly disease in which antibody-producing cells aberrantly churn out abnormal protein fibers comprised of antibody light chains. These fibers aggregate to form amyloid deposits that damage the organs and tissues in which they accumulate. As such, AL amyloidosis can manifest with a variety of symptoms. But among them, heart dysfunction and low blood pressure tend to indicate a poorer prognosis. Because vascular dysfunction can contribute to hypotension, Stamatelopoulos and colleagues examined vascular health via flow-mediated vasodilation (FMD)—a measure of brachial artery diameter after brief lower arm ischemia—in 115 newly diagnosed AL patients. While a high FMD normally indicates a healthy vascular response, in AL patients, FMD was higher than in age-, sex-, and cardiovascular risk factor-matched controls. Moreover, this high FMD in patients was strongly predictive of mortality in the subsequent months and years of follow up. High FMD was more predictive of death, in fact, than some other measures of cardiovascular health. The results suggest that FMD may be a superior means for identifying AL patients most at risk, and for assessing potential benefits of therapeutic interventions.Circulating MCP-1 Levels and Incident Stroke (p 773)Download figureDownload PowerPointHigh MCP-1 levels are linked to increased risk of stroke, report Georgakis et al.Atherosclerosis, which increases a person’s risk of suffering a myocardial infarction or ischemic stroke, is a chronic inflammatory disease. As such, inhibiting the activity of proinflammatory cytokines is a potential therapeutic strategy to slow disease progression. One such cytokine under study is MCP-1 (monocyte chemoattractant protein 1). Animal studies have shown that blocking or boosting MCP-1 limits or accelerates atherosclerosis, respectively. Large-scale observational studies of MCP-1 in humans have been lacking, however. To rectify this, Georgakis and colleagues performed a meta analysis of previously unpublished data from 6 population cohorts totaling 17 180 individuals who were followed for an average of 16.3 years. From this data, the team identified a significant association between high base-line MCP-1 levels and the likelihood of suffering a future ischemic stroke. There was no such association with hemorrhagic stroke, which is not typically caused by atherosclerosis. The result supports the previous animal studies as well as a recent human study that showed genetic predisposition for high levels of MCP-1 was associated with increased risk of coronary artery disease and stroke. It also suggests that therapeutic interventions to lower MCP-1 activity may indeed warrant investigation. Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesReactive Vasodilation Predicts Mortality in Primary Systemic Light-Chain AmyloidosisKimon Stamatelopoulos, et al. Circulation Research. 2019;125:744-758Miro2 Regulates Inter-Mitochondrial Communication in the Heart and Protects Against TAC-Induced Cardiac DysfunctionYangpo Cao, et al. Circulation Research. 2019;125:728-743Circulating Monocyte Chemoattractant Protein-1 and Risk of StrokeMarios K. Georgakis, et al. Circulation Research. 2019;125:773-782 September 27, 2019Vol 125, Issue 8 Advertisement Article InformationMetrics © 2019 American Heart Association, Inc.https://doi.org/10.1161/RES.0000000000000301PMID: 31557124 Originally publishedSeptember 26, 2019 PDF download Advertisement