HomeCirculation ResearchVol. 128, No. 2In This Issue Free AccessIn BriefPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessIn BriefPDF/EPUBIn This Issue Ruth Williams Ruth WilliamsRuth Williams Search for more papers by this author Originally published21 Jan 2021https://doi.org/10.1161/RES.0000000000000461Circulation Research. 2021;128:151is related toLoss of Endogenously Cycling Adult Cardiomyocytes Worsens Myocardial FunctionEosinophils Protect Mice From Angiotensin-II Perfusion–Induced Abdominal Aortic AneurysmMachine Learned Cellular Phenotypes in Cardiomyopathy Predict Sudden DeathKlotho Deficiency Causes Heart Aging via Impairing the Nrf2-GR PathwayJNK2, a Newly-Identified SERCA2 Enhancer, Augments an Arrhythmic [Ca2+]SR Leak-Load RelationshipSIRT6 Protects Smooth Muscle Cells From Senescence and Reduces AtherosclerosisIdentifying Cycling Cardiomyocytes In Vivo (p 155)Bradley et al develop a transgenic mouse for identifying cycling cells in the adult heart.Download figureDownload PowerPointIn general, the heart muscle cells of mammals stop proliferating soon after birth and become terminally differentiated. It is therefore believed that after a heart attack, cardiomyocyte proliferation makes a minimal contribution, if any, to the repair. Instead, the lost cardiomyocytes are replaced with a non-functional fibrotic scar, which may eventually lead to heart failure. The true extent of post-injury cardiomyocyte proliferation is unknown, however, because tools for identifying cycling heart cells are limited, say Bradley and colleagues. Some only identify cells at a particular point in the cell cycle, and may therefore underestimate proliferation, while those that mark DNA replication identify both divided and polyploid cells. Bradley and colleagues therefore developed a novel inducible transgenic mechanism to create mice in which all adult cardiomyocytes reentering the cell cycle are labeled. Using the system, they showed that cardiomyocytes did increase DNA replication after injury, but this was rarely associated with cell division. Nevertheless, ablation of this injury-induced cell cycling caused mice to fair worse after myocardial infarction, the team found, suggesting such newly cycling cells are somehow beneficial for tissue recovery and deserve further study.Computational Phenotypes for VT/VF Risk (p 172)Ventricular action potential phenotypes predict outcomes of ischemic cardiomyopathy patients, say Rogers et al.Download figureDownload PowerPointPatients with ischemic cardiomyopathy (IC)—a weakening of the heart muscles caused by reduced blood oxygen supply—are at an increased risk of sudden cardiac arrest. However, it is hard to predict which patients are the most at risk and would therefore benefit from additional interventions, such as implanted cardiac defibrillators. In an attempt to stratify IC patients based on risk, Rogers and colleagues took electrophysiological recordings from patients’ hearts and used them, together with the 3-year outcomes of the patients, to train a machine-learning algorithm. Over 5,000 action potential recordings were made in 42 patients, the data from 29 being used for training the algorithm, and that of the remaining 13 being used for testing its prediction ability. Over the three years, 13 of the patients developed arrhythmias and 14 died. The study revealed that early repolarization of action potentials was a predictor of mortality, while prolonged phase II repolarization predicted arrhythmia development. In fact, the computational prediction outperformed established predictors such as comorbidites and measures of heart function, suggesting that such recordings could aid in directing personalized management and intervention decisions for IC patients.Eosinophils in Abdominal Aortic Aneurysm (p 188)Liu et al report and unexpected role of eosinophils in aortic aneurysms.Download figureDownload PowerPointThere are many risk factors associated with developing an abdominal aortic aneurysm (AAA)—a life threatening ballooning of the aorta that can lead to the vessel’s rupture. People with asthma, for example, have a two-fold risk of AAA compared to those without. Because patients with severe asthma tend to have high numbers of eosinophils, and because high numbers of eosinophils have been tied to other cardiovascular issues, Liu and colleagues thought these cells might be behind the aneurysm risk. They compared 579 AAA patients with 5,063 healthy controls, finding higher numbers of eosinophils in the AAA group. They also found high eosinophil numbers in AAA lesions compared with normal vessels in both mice and humans. The team went on to create mice that lacked eosinophils, but when they induced aneurysms in these animals, they got a surprise. In the absence of eosinophils, the aneurysms were exacerbated, with more inflammatory cells and cytokines detected than in the lesions of control animals. Furthermore, transfer of eosinophils from wild type mice to the eosinophil-deficient animals blocked aneurysm growth. The team concludes that eosinophils actually protect against aneurysm growth and suggest boosting the beneficial effects of these cells may be a novel strategy for aneurysm treatment. Previous Back to top Next FiguresReferencesRelatedDetailsRelated articlesLoss of Endogenously Cycling Adult Cardiomyocytes Worsens Myocardial FunctionLeigh A. Bradley, et al. Circulation Research. 2021;128:155-168Eosinophils Protect Mice From Angiotensin-II Perfusion–Induced Abdominal Aortic AneurysmCong-Lin Liu, et al. Circulation Research. 2021;128:188-202Machine Learned Cellular Phenotypes in Cardiomyopathy Predict Sudden DeathAlbert J. Rogers, et al. Circulation Research. 2021;128:172-184Klotho Deficiency Causes Heart Aging via Impairing the Nrf2-GR PathwayKai Chen, et al. Circulation Research. 2021;128:492-507JNK2, a Newly-Identified SERCA2 Enhancer, Augments an Arrhythmic [Ca2+]SR Leak-Load RelationshipJiajie Yan, et al. Circulation Research. 2021;128:455-470SIRT6 Protects Smooth Muscle Cells From Senescence and Reduces AtherosclerosisMandy O.J. Grootaert, et al. Circulation Research. 2021;128:474-491 January 22, 2021Vol 128, Issue 2Article InformationMetrics Download: 509 © 2021 American Heart Association, Inc.https://doi.org/10.1161/RES.0000000000000461 Originally publishedJanuary 21, 2021 PDF download