{"title":"Turn(over) the Page","authors":"Thomas G. Martin PhD , Leslie A. Leinwand PhD","doi":"10.1016/j.jacbts.2024.05.002","DOIUrl":"https://doi.org/10.1016/j.jacbts.2024.05.002","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"9 6","pages":"Pages 808-810"},"PeriodicalIF":8.4,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X24001876/pdfft?md5=b89b3ec9289a3d23dbc1a23f3678e48a&pid=1-s2.0-S2452302X24001876-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141481417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Douglas L. Mann MD (Editor-in-Chief, JACC: Basic to Translational Science)
{"title":"Remembering Ada L. Steininger","authors":"Douglas L. Mann MD (Editor-in-Chief, JACC: Basic to Translational Science)","doi":"10.1016/j.jacbts.2024.05.004","DOIUrl":"https://doi.org/10.1016/j.jacbts.2024.05.004","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"9 6","pages":"Page 844"},"PeriodicalIF":8.4,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X2400189X/pdfft?md5=ebfd16973328dba6319e0a3cee6ff63c&pid=1-s2.0-S2452302X2400189X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141481415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Coordinate Targeting of Mitochondrial Energetics, Antioxidant Defenses, and Inflammation","authors":"Michael N. Sack MD, PhD","doi":"10.1016/j.jacbts.2024.02.013","DOIUrl":"https://doi.org/10.1016/j.jacbts.2024.02.013","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"9 6","pages":"Pages 751-753"},"PeriodicalIF":8.4,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X24000913/pdfft?md5=2435a024ae847b02f4d71c9a359b3743&pid=1-s2.0-S2452302X24000913-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141480664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"New Drug-Coated Balloons on the Horizon","authors":"Bernardo Cortese MD","doi":"10.1016/j.jacbts.2024.04.001","DOIUrl":"https://doi.org/10.1016/j.jacbts.2024.04.001","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"9 6","pages":"Pages 790-791"},"PeriodicalIF":8.4,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X24001384/pdfft?md5=593da5cd10509b9c553adb04ca008ef8&pid=1-s2.0-S2452302X24001384-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141481414","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Katrin Nitz PhD , Joerg Herrmann MD , Amir Lerman MD , Esther Lutgens MD, PhD
{"title":"Costimulatory and Coinhibitory Immune Checkpoints in Atherosclerosis","authors":"Katrin Nitz PhD , Joerg Herrmann MD , Amir Lerman MD , Esther Lutgens MD, PhD","doi":"10.1016/j.jacbts.2023.12.007","DOIUrl":"10.1016/j.jacbts.2023.12.007","url":null,"abstract":"<div><p>The benefits of current state-of-the-art treatments to combat atherosclerotic cardiovascular disease (ASCVD) have stagnated. Treatments are mostly based on controlling cardiovascular risk factors, especially hyperlipidemia. Although the most recent advances with PCSK-9 inhibitors support the hyperlipidemia aspect of ASCVD, several lines of experimental evidence have outlined that atherosclerosis is also driven by inflammation. In the past years, phase 1, 2, and 3 clinical trials targeting inflammation to combat ASCVD have revealed that patients do tolerate such immune therapies, show decreases in inflammatory markers, and/or have reductions in cardiovascular endpoints. However, the search for the optimal anti-inflammatory or immune-modulating strategy and the stratification of patients who would benefit from such treatments and appropriate treatment regimens to combat ASCVD is only just beginning. In this review, we focus on immune checkpoint–based therapeutics (costimulation and coinhibition), many of which are already approved by the U.S. Food and Drug Administration for the treatment of cancer or autoimmune diseases, and discuss their use as a novel immunotherapeutic strategy to treat ASCVD.</p></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"9 6","pages":"Pages 827-843"},"PeriodicalIF":8.4,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X24000044/pdfft?md5=543b74fb6a4778f1f4dffdad9ab5fdce&pid=1-s2.0-S2452302X24000044-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140271122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiao Sun PhD , Wei Chen MD, PhD , Alexander C. Razavi MD, PhD, MPH , Mengyao Shi PhD, MPH , Yang Pan PhD , Changwei Li MD, PhD , Maria Argos PhD , Brian T. Layden MD , Martha L. Daviglus MD, PhD , Jiang He MD, PhD , Owen T. Carmichael PhD , Lydia A. Bazzano MD, PhD , Tanika N. Kelly PhD, MPH
{"title":"Associations of Epigenetic Age Acceleration With CVD Risks Across the Lifespan","authors":"Xiao Sun PhD , Wei Chen MD, PhD , Alexander C. Razavi MD, PhD, MPH , Mengyao Shi PhD, MPH , Yang Pan PhD , Changwei Li MD, PhD , Maria Argos PhD , Brian T. Layden MD , Martha L. Daviglus MD, PhD , Jiang He MD, PhD , Owen T. Carmichael PhD , Lydia A. Bazzano MD, PhD , Tanika N. Kelly PhD, MPH","doi":"10.1016/j.jacbts.2024.01.018","DOIUrl":"10.1016/j.jacbts.2024.01.018","url":null,"abstract":"<div><p>Although epigenetic age acceleration (EAA) might serve as a molecular signature of childhood cardiovascular disease (CVD) risk factors and further promote midlife subclinical CVD, few studies have comprehensively examined these life course associations. This study sought to test whether childhood CVD risk factors predict EAA in adulthood and whether EAA mediates the association between childhood CVD risks and midlife subclinical disease. Among 1,580 Bogalusa Heart Study participants, we estimated extrinsic EAA, intrinsic EAA, PhenoAge acceleration (PhenoAgeAccel), and GrimAge acceleration (GrimAgeAccel) during adulthood. We tested prospective associations of longitudinal childhood body mass index (BMI), blood pressure, lipids, and glucose with EAAs using linear mixed effects models. After confirming EAAs with midlife carotid intima-media thickness and carotid plaque, structural equation models examined mediating effects of EAAs on associations of childhood CVD risk factors with subclinical CVD measures. After stringent multiple testing corrections, each SD increase in childhood BMI was significantly associated with 0.6-, 0.9-, and 0.5-year increases in extrinsic EAA, PhenoAgeAccel, and GrimAgeAccel, respectively (<em>P</em> < 0.001 for all 3 associations). Likewise, each SD increase in childhood log-triglycerides was associated with 0.5- and 0.4-year increases in PhenoAgeAccel and GrimAgeAccel (<em>P</em> < 0.001 for both), respectively, whereas each SD increase in childhood high-density lipoprotein cholesterol was associated with a 0.3-year decrease in GrimAgeAccel (<em>P</em> = 0.002). Our findings indicate that PhenoAgeAccel mediates an estimated 27.4% of the association between childhood log-triglycerides and midlife carotid intima-media thickness (<em>P</em> = 0.022). Our data demonstrate that early life CVD risk factors may accelerate biological aging and promote subclinical atherosclerosis.</p></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"9 5","pages":"Pages 577-590"},"PeriodicalIF":9.7,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X24000500/pdfft?md5=50ec6dd3ed97ff03b56d56219d0b34c1&pid=1-s2.0-S2452302X24000500-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140786732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"miR-590-3p Overexpression Improves the Efficacy of hiPSC-CMs for Myocardial Repair","authors":"Zhiwei Zhang MD , Xiaoting Li MD , Jiawei Zhuang MD , Qingwei Ding MD , Hui Zheng MD , Teng Ma MD , Qingyou Meng MD , Ling Gao PhD","doi":"10.1016/j.jacbts.2023.11.005","DOIUrl":"10.1016/j.jacbts.2023.11.005","url":null,"abstract":"<div><p>Recent evidence demonstrates that low engraftment rates limit the efficacy of human induced pluripotent stem cell–derived cardiomyocytes (hiPSC-CMs) for cardiac repair after myocardial infarction. In this study, we attempted to overcome this limitation by enhancing the proliferative capacity of transplanted hiPSC-CMs. We found that miR-590-3p overexpression increased the proliferative capacity of hiPSC-CMs. miR-590-3p overexpression increased the number of engrafted cells and had a higher efficacy for myocardial repair than control cells. Moreover, we confirmed the safety of using miR-590-3p-overexpressing hiPSC-CMs in pig hearts. These results indicated that miR-590-3p overexpression stimulated hiPSC-CM cell cycle re-entry to induce cell proliferation and increased the therapeutic efficacy in MI.</p></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"9 5","pages":"Pages 557-573"},"PeriodicalIF":9.7,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X23005193/pdfft?md5=06e86e28db0c5b4549397c70e494adf9&pid=1-s2.0-S2452302X23005193-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139880823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}