JACC-Basic to Translational ScienceJACC：基础与转化科学
JACC-Basic to Translational Science(英文缩写 JACC-BASIC TRANSL SC),ISSN 2452-302X,eISSN 2452-302X,中文译名:JACC：基础与转化科学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 9.531 | Q1 |
| 2022 | 9.700 | Q1 |
| 2023 | 8.400 | Q1 |
| 2024 | 7.200 | Q1 |
| 2025 | 8.400 | Q1 |
JACC-Basic to Translational Science 最新收录文献
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1. Decreased Endothelial Cell Retinoic Acid Signaling Accelerates Progression of Single Ventricle Pulmonary Vascular Malformations.
PMID:日期:2026-09-24Pulmonary vascular malformations (PVMs) are vascular complications that universally develop in patients with single ventricle congenital heart disease after Glenn surgery, yet the pathogenesis of single ventricle PVMs remains unknown. Using a surgical rat model of Glenn circulation, single-cell RNA sequencing (scRNAseq) on whole lung samples identified dramatic endothelial cell (EC) gene expression changes post-surgery, including decreased all-trans retinoic acid (ATRA) signaling. Many gene expression differences (∼17% of all EC differentially expressed genes), including decreased ATRA signaling, were shared with 2 independent models of hereditary hemorrhagic telangiectasia arteriovenous malformations (AVMs). Subsequent dietary modification of vitamin A (Vit A) intake in rats, identified that dietary deficiency of Vit A increased PVM shunting severity, which was mitigated with excess dietary Vit A intake. Collectively, our study of post-Glenn PVMs identified shared patho-mechanisms with hereditary hemorrhagic telangiectasia AVMs, including decreased EC ATRA signaling, which is a novel potential target for treating AVMs.
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3. Casting Light on the Regulation of Platelet Reactivity by Calcitriol.
PMID:日期:2026-09-22该文献暂无摘要。
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5. Dapagliflozin Prevents Heart Failure With Preserved Ejection Fraction by Inhibiting the Sodium/Hydrogen Exchanger.
PMID:日期:2026-09-18Sodium-glucose cotransporter 2 (SGLT2) inhibitors have shown protective effects against heart failure with preserved ejection fraction (HFpEF), but SGLT2 is not expressed significantly in the heart. Here, we investigated the mechanism by which the SGLT2 inhibitor dapagliflozin (Dapa) alters HypoMg-associated HFpEF. HypoMg was induced by a low-Mg diet in mice or in a human cardiomyocyte cell line. Three weeks of Dapa treatment prevented HypoMg-induced HFpEF in mice. In RL-14 cardiomyocytes, sodium-hydrogen exchanger 1 (NHE1) overexpression or activation mimicked the cellular effects of HypoMg. Dapa reversed these changes. Dapa prevented cardiac HFpEF by inhibiting cardiomyocyte NHE1 activity and suppressing macrophage activation.
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7. A Novel Triglyceride- and Cholesterol-Enriched Lipoprotein(a) Phenotype in Moderate Hypertriglyceridemia: Reversal by ApoC-III Inhibition.
PMID:日期:2026-09-17In moderate hypertriglyceridemia, lipoprotein(a) (Lp[a]) particles were enriched in triglycerides and cholesterol, accounting for about 16% to 21% of plasma triglycerides and about 9% to 11% of plasma cholesterol. In a phase 2 trial, apolipoprotein C-III inhibition with olezarsen reduced Lp(a)-associated triglycerides and cholesterol by about 56% to 70%, with no consistent reduction in plasma Lp(a). Oxidized phospholipid measures tracked more closely with Lp(a) particle concentration than with Lp(a)-associated lipid content, supporting partially distinct dimensions of Lp(a) biology. These findings identify Lp(a) lipid composition as a dynamic, therapeutically modifiable feature in hypertriglyceridemia. (Study of ISIS 678354 [AKCEA-APOCIII-LRx] in Participants With Hypertriglyceridemia and Established Cardiovascular Disease [CVD]; NCT03385239).
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9. Spatially Distinct Bone Marrow Sites Are Asymmetrically Impacted by Inflammatory Cardiovascular Disease.
PMID:日期:2026-09-16Cardiovascular disease, a leading cause of mortality globally, is increasingly recognized to involve complex bone marrow-driven inflammatory mechanisms, yet the impact on spatially distinct bone marrow sites and comorbidities remains poorly understood. To address this, we developed MarrowMet, a methodology for whole-body, site-specific quantification of bone marrow activity. The approach involves intravenously injecting the metabolic tracer 18F-fluorodeoxyglucose (F-FDG) in mice, followed by bone excision to quantify site-specific bone marrow activity, with values then superimposed on a whole-body mouse atlas. After establishing that F-FDG bone marrow uptake strongly correlated with inflammatory activity, we applied MarrowMet to map site-specific activation patterns across diverse cardiovascular pathologies, including mouse models of inflammatory atherosclerosis, acute ischemic events, acute respiratory distress syndrome, metabolic syndrome, and aging. MarrowMet guided the selection of bone marrow regions of interest for in-depth mass cytometric analyses, with the skull and sternum emerging as critical sites exhibiting distinct immune and metabolic profiles in cardiovascular disease. These results challenge the prevailing view that femoral marrow represents systemic activity. Together, this work lays a foundation for whole-body exploration of bone marrow heterogeneity, yielding critical insights into cardiovascular disease and associated inflammatory responses, and MarrowMet can be readily adopted to profile other immune mechanisms in a variety of pathologies, including cancer and autoimmune diseases.
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10. Reply: IL-1 Blockade to Resolve Persistent Inflammation After STEMI.
PMID:日期:2026-09-14该文献暂无摘要。