Circulation Research

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Blocking mmu-miR-721 in experimental autoimmune myocarditis mice increases Pparg, lowers RORγt/IL-17 activity, reduces cardiac leukocyte infiltration, and improves cardiac function.

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NNMT expression is inversely associated with older, plaque-adjacent human carotid intimal status, and restoring NNMT in aged mice improves vasodilation and arterial stiffness.

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Exercise in mice increases skeletal muscle-derived small extracellular vesicle entry into the heart, and these sEVs significantly attenuate myocardial ischemia/reperfusion injury.

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Endothelial KLK8 is strongly upregulated in streptozotocin-induced diabetic mice and high-glucose–treated glomerular endothelial cells, and its loss improves albuminuria and glomerular pathology.

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Oral potassium chloride (KCl) supplementation for 6–9 weeks eliminated the muscle Na+ surplus in hyperaldosteronism, with a -1.90 mmol/L tissue volume reduction.

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Hypertension markedly elevates cerebral endothelial Piezo1 activity in two mouse models, and endothelial Piezo1 deletion protects against impaired vasomotion and functional hyperemia.

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MOF is increased in aortic monocyte/macrophages in human abdominal aortic aneurysms and is linked to inflammatory transcriptional programs, with TNF-α driving MOF induction.

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CaMKIIδ-dependent TRPC6 membrane externalization in resistance-sized small mesenteric artery VSMCs is linked to enhanced RyR Ca2+ sparks and BKCa currents specifically in old (12–14 months) mice.

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Myeloid-specific deletion of calprotectin (CPT) in CKD-mineral and bone disorder mice significantly attenuates aortic calcification and osteogenic signaling while shifting circulating CPPs toward an immature fraction.

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Sunitinib treatment of iPSC-derived cardiomyocytes from 20 healthy donors shows donor-resolved heterogeneity, with relaxation velocity most consistently linked to cardiotoxicity severity.

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In pulmonary artery banded pigs, worsening right ventricular dysfunction from RV ejection fraction 38±4% to 20±8% is linked to distinct cellular programs and targetable stress pathways.

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Endothelial-specific RUNX3 knockout mice show hypersprouting retinal angiogenesis with reduced DLL4 expression and impaired vascular integrity, including lower VE-cadherin and claudin-5.

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Arterial endothelial cell–derived CSF1 is essential for maintaining intimal tissue-resident macrophages in healthy aortas and in 4-week foam cell lesions of Ldlr-/- mice.

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CD36 deficiency in mice disrupts circadian blood pressure rhythms, producing significantly higher daytime BP, and platelet CD36 levels are linked to nocturnal hypertension severity in humans.

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BAHCC1 is upregulated in human restenotic and atherosclerotic arteries and rat arteries with IH, and its H3K27me3 binding supports neointima formation in injury models.

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In a CKD-hyperlipidemia mouse model, SMC DDR1 mechanosensing links arterial stiffening to higher THBS1, worsening atherosclerotic burden.

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CD4+ T-cell–derived IFNγ drives LOXL3-dependent ECM stiffening in cardiac fibroblasts, and disrupting this axis attenuates adverse remodeling and improves diastolic function in a murine cardiometabolic HFpEF model.

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Glutaminolysis rapidly mobilizes during acute β-adrenergic stress in mouse hearts to supply mitochondrial glutathione, preserving redox balance and sustaining contractile reserve.

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RBFOX2 dosage is essential for cardiomyocyte differentiation, where heterozygous cells fail to reach autoregulatory splicing thresholds, producing aberrant isoforms and reducing functional RBFOX2 below 50% of wild-type.

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NK cell–specific loss of TGF-β receptor signaling in neonatal mice (Tgfbr2 NK-/-) reduces distal arteriolar density and impairs alveolarization, with sex-specific long-term lung function deficits.

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Reduced Ca2+ spark frequency in pressurized omental resistance arteries from women with preeclampsia is linked to lower spontaneous transient outward currents and impaired sarcoplasmic reticulum Ca2+ handling.

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CCR2-dependent monocyte recruitment is linked to progression from post-MI heart failure to pulmonary hypertension in mice, with RS102895 reducing lung vascular remodeling by 6 weeks.

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BAFF is significantly upregulated in SLE-PAH, and BAFF overexpression in humanized BAFF-transgenic mice drives a S100a6+ mature B-cell subset that triggers endothelial apoptosis and pulmonary vascular remodeling.