JACC: Basic to Translational Science最新文献

{"title":"Closing the Loop on Right Ventricular Mechanics","authors":"Alessio Alogna MD, PhD","doi":"10.1016/j.jacbts.2025.101361","DOIUrl":"10.1016/j.jacbts.2025.101361","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 8","pages":"Article 101361"},"PeriodicalIF":8.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144896125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiac TRPM7 Causes Diabetic Heart Failure With Preserved Ejection Fraction","authors":"Man Liu PhD,&nbsp;Hong Liu MD, PhD,&nbsp;Gyeoung-Jin Kang PhD,&nbsp;Lynn M. Hartweck PhD,&nbsp;Feng Feng BS,&nbsp;Eunji Kim PhD,&nbsp;Kurt W. Prins MD, PhD,&nbsp;Samuel C. Dudley Jr. MD, PhD","doi":"10.1016/j.jacbts.2025.101321","DOIUrl":"10.1016/j.jacbts.2025.101321","url":null,"abstract":"<div><div>Hypomagnesemia (HypoMg) and subsequent oxidative stress cause diabetic cardiac diastolic dysfunction and heart failure with preserved ejection fraction. A Mg²⁺ transporter with channel and kinase function, transient receptor potential cation channel subfamily M 7 (TRPM7), is upregulated in HypoMg. Diabetes mellitus mice had HypoMg and elevated TRPM7 expression in the heart. TRPM7 kinase mediated mitochondrial dysfunction and cardiac diastolic dysfunction in HypoMg. TRPM7 kinase enhanced mitochondrial Fgr expression, with subsequent complex II dysfunction and mitochondrial reactive oxygen species overproduction. Inhibition of TRPM7 kinase represents a potential novel therapeutic strategy to treat diabetic heart failure with preserved ejection fraction.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 8","pages":"Article 101321"},"PeriodicalIF":8.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144896124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recognizing Early Career Translational Investigators","authors":"Matthias Nahrendorf MD, PhD (Editor-in-Chief: JACC: Basic to Translational Science)","doi":"10.1016/j.jacbts.2025.101362","DOIUrl":"10.1016/j.jacbts.2025.101362","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 8","pages":"Article 101362"},"PeriodicalIF":8.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144896129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unleashing the Power of the Beehive to Begin a New Era for JACC: Basic to Translational Science","authors":"Matthias Nahrendorf MD, PhD (Editor-in-Chief, JACC: Basic to Translational Science)","doi":"10.1016/j.jacbts.2025.101360","DOIUrl":"10.1016/j.jacbts.2025.101360","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 8","pages":"Article 101360"},"PeriodicalIF":8.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144896131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knockdown of PARM1 Alleviates Aortic Valve Calcification via the PRKCH-MAPK Signaling Pathway","authors":"Haochang Hu PhD ,&nbsp;Xian Zhu MD ,&nbsp;Jinyong Chen PhD ,&nbsp;Naifang Cao PhD ,&nbsp;Shuangshuang Yang MD ,&nbsp;Lan Xie PhD ,&nbsp;Wangxing Hu PhD ,&nbsp;Si Cheng PhD ,&nbsp;Juan Fang MD ,&nbsp;Yi Qian PhD ,&nbsp;Dilin Xu PhD ,&nbsp;Ningjing Qian MD ,&nbsp;Dao Zhou MD ,&nbsp;Jin Lu MD ,&nbsp;Hanyi Dai MD ,&nbsp;Junhui Xue PhD ,&nbsp;Wei Zhu MD ,&nbsp;Jian’an Wang MD, PhD ,&nbsp;Xianbao Liu MD, PhD","doi":"10.1016/j.jacbts.2025.02.019","DOIUrl":"10.1016/j.jacbts.2025.02.019","url":null,"abstract":"<div><div>With the aging of the population, the prevalence of calcific aortic valve disease (CAVD) has increased yearly. However, effective means to delay or even reverse the progression of CAVD are still lacking. This study revealed that prostate androgen-regulated mucin-like protein 1 (PARM1) expression was significantly up-regulated in calcified aortic valve tissues. Functional investigations demonstrated that PARM1 knockdown effectively suppressed osteogenic differentiation of valvular interstitial cells (VICs) and mitigated pathological aortic valve calcification. Mechanically, PARM1 knockdown down-regulated PRKCH mRNA expression, consequently attenuating MAPK pathway activation during the osteogenic differentiation of VICs. In conclusion, PARM1 could be a feasible target for CAVD prevention.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 8","pages":"Article 101260"},"PeriodicalIF":8.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144173821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Towards Mechanism-Based Therapies in Arrhythmogenic Cardiomyopathy","authors":"Jeffrey E. Saffitz MD, PhD","doi":"10.1016/j.jacbts.2025.05.008","DOIUrl":"10.1016/j.jacbts.2025.05.008","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 8","pages":"Article 101313"},"PeriodicalIF":8.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144896069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Full Issue PDF","authors":"","doi":"10.1016/S2452-302X(25)00321-3","DOIUrl":"10.1016/S2452-302X(25)00321-3","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 8","pages":"Article 101368"},"PeriodicalIF":8.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144896070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Congenital Heart Diseases and Neurodevelopmental Disorders","authors":"Marie Demonceaux PhD ,&nbsp;Oscar Werner MD ,&nbsp;Olivier Cadeau PsyD, PhD ,&nbsp;Amanda Guerra PsyD, PhD ,&nbsp;Arnaud Roy PsyD, PhD ,&nbsp;Véronique Ferchaud-Roucher PhD ,&nbsp;Alban-Elouen Baruteau MD, PhD","doi":"10.1016/j.jacbts.2025.01.022","DOIUrl":"10.1016/j.jacbts.2025.01.022","url":null,"abstract":"<div><div>Congenital heart disease (CHD) is the primary cause of birth defects, affecting 9 per 1,000 live births. Up to 50% of them will develop neurodevelopmental disorders, two-thirds of which being unexplained by postnatal risk factors. Recent advances suggest a triangular relationship between the placenta and the fetal heart and brain in CHD, consistent with the Developmental Origins of Health and Disease hypothesis, ie, the in utero programming of early and later-in-life noncommunicable cardiometabolic and mental diseases. The current review provides comprehensive evidence of placental, cardiac, and cerebral tissues interactions, and details how placental dysregulation may affect vasculogenesis, angiogenesis and neural tube closure, hemodynamics, energy supply, endocrine function, and epigenetic regulation of the developing heart and brain. Future studies should include placental research, since identifying placental biomarkers would allow early identification of CHD infants at higher risk for neurodevelopmental disorders, leading to targeted preventive personalized interventions.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 8","pages":"Article 101251"},"PeriodicalIF":8.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144021211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increased Generation of Hypoxanthine","authors":"Katrin Schäfer MD","doi":"10.1016/j.jacbts.2025.101320","DOIUrl":"10.1016/j.jacbts.2025.101320","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 8","pages":"Article 101320"},"PeriodicalIF":8.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144896127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Controlled Right Ventricular Pressure Overload Can Rescue Left Ventricular Dysfunction by Promoting Biventricular Adaptive Hypertrophy","authors":"Matteo Ponzoni MD ,&nbsp;Azadeh Yeganeh PhD ,&nbsp;Libo Zhang MD ,&nbsp;Jennifer Zhang MD, PhD ,&nbsp;Ramesh B. Vanama PhD ,&nbsp;Kaley Hogarth MBS ,&nbsp;Quynh N. Phi BSc ,&nbsp;Jing Li MD, PhD ,&nbsp;Loukmane Karim PhD ,&nbsp;John G. Coles MD ,&nbsp;Jason T. Maynes MD, PhD","doi":"10.1016/j.jacbts.2025.02.018","DOIUrl":"10.1016/j.jacbts.2025.02.018","url":null,"abstract":"<div><div>Pulmonary artery banding (PAB) has been investigated as a therapy for left ventricular (LV) dysfunction in pediatric dilated cardiomyopathy; however, the underlying mechanisms of action of PAB-induced LV rehabilitation remain unknown. This study aims to establish a small animal model of PAB-treated LV dysfunction to document the biventricular hemodynamic and tissue-level modifications promoted by PAB. Sprague-Dawley rats underwent left anterior descending (LAD) artery ligation (LV dysfunction model) followed by PAB 1-week post-injury (LAD + PAB, n = 13). Controls consisted of sham (n = 16), PAB-only (n = 16), and LAD rats (n = 15). The animals underwent weekly echocardiography and terminal histopathology 4 weeks after surgery. Data shown as mean ± SEM or median (Q1-Q3). LAD + PAB rats exhibited positive LV remodeling (LV end-diastolic volume: 0.49 ± 0.02 mL vs 0.66 ± 0.03 mL; <em>P</em> &lt; 0.001), improvement of LV ejection fraction (0.48 ± 0.01 vs. 0.36 ± 0.01; <em>P</em> &lt; 0.001), and normalization of mitral valve Doppler E/A (1.43 ± 0.03 vs 1.91 ± 0.09; <em>P</em> &lt; 0.001) compared to LAD animals. Histologic analysis documented LV hypertrophy (wall thickness/body weight: 9.3 ± 0.4 μm/g vs 7.2 ± 0.3 μm/g; <em>P</em> = 0.005), increased LV cardiomyocyte diameter (14.8 [Q1-Q3: 13.9-15.7] μm vs 11.3 [Q1-Q3: 10.8-11.7] μm; <em>P</em> = 0.001), and augmented neoangiogenesis (6.5 ± 0.2 vessels/mm² vs 4.7 ± 0.5 vessels/mm²; <em>P</em> = 0.005) in LAD + PAB vs LAD hearts. Mechanistically, we observed reduced LV fibrosis (9.8% [Q1-Q3: 7.7%-13.4%] vs 17.4% [Q1-Q3: 14.8%-20.2%]; <em>P</em> = 0.003) and fibroblast cellular senescence (5.7% [Q1-Q3: 4%-10.7%] vs 16.1% [7.6%-18.4%], <em>P</em> = 0.029), and preserved phospholamban (PLN) phosphorylation in the LV of LAD + PAB vs LAD rats (increased PLN/PLN: 0.6 ± 0.1 vs 1.0 ± 0.1; <em>P</em> = 0.008). In our model, PAB induced positive LV remodeling and improved LV systolic-diastolic function. PAB stimulated biventricular compensated hypertrophy that may constitute a potential adaptive mechanism which can rescue residual LV function and limit LV fibrosis/injury.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 8","pages":"Article 101259"},"PeriodicalIF":8.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144325774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}