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Joined February 2012
5,836 Photos and videos
ABYSS Trial Analysis: Higher resting heart rate predicts adverse events post-MI regardless of ejection fraction. β-blocker discontinuation raises heart rate by 10–13 bpm and worsens outcomes consistently across baseline heart rate tertiles ahajrnls.org/3S1HoDC
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Endothelial SHMT2 drives pulmonary vascular remodeling via the SHMT2–BRISC–RhoB axis. Namodenoson inhibits this pathway with in vivo efficacy and an established clinical safety profile.ahajrnls.org/4e7mDij
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RND3 was identified as a novel mitochondrial matrix-resident small GTPase essential for energy metabolism homeostasis and normal cardiac function, with potential as a therapeutic target in ischemia-reperfusion injury.ahajrnls.org/4fD4OsF
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In a multicenter PET registry, patients with no evidence of flow-limiting CAD and discordantly low subendocardial myocardial flow reserve (MFR) had an increased risk of MACE than those with normal transmural & subendocardial MFR. ahajrnls.org/444SnyD
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Mutations in Notch transcriptional coactivator MAML1 directly recapitulated VSDs in models. Dysregulation of liquid-liquid phase separation impaired Notch signaling, establishing link between condensate dynamics & congenital disease. ahajrnls.org/4e8WQ9G
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Alternative splicing of Tropomyosin 1 (TPM1b) exon 9a is a pathogenic mechanism in myofilament disorder and diastolic dysfunction in HFpEF and is mediated by SRPK3. This may represent a novel therapeutic target for HFpEF.ahajrnls.org/4fHNsLl
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HIF-2 drives coronary inflammation, remodeling, and thrombosis in a novel mouse model recapitulating Kawasaki disease. Pharmacological HIF-2 targeting may be a new therapeutic strategy for coronary vasculitis. ahajrnls.org/3S50B7j
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Common African ancestry-enriched variants of uncertain significance associated with increased cardiomyopathy and arrhythmia risk, particularly in individuals with CV risk factors or HF. ahajrnls.org/4gcmFXC
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SREBP1 transactivates NHE3 in cardiomyocytes during HFpEF, leading to calcium mishandling and impaired contractility in heart failure.ahajrnls.org/43wymRC
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Sam68, a stress-activated cardiomyocyte scaffold, drives pathological cardiac hypertrophy by scaffolding Src–STAT3 to induce PDK4 and suppressing cardiomyocyte glucose Oxidation ahajrnls.org/4uzqoSD
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#ResearchLetter: Locally deployed LLMs accurately adjudicate heart failure hospitalizations at cardiologist-level accuracy, as an approach to reduce cardiovascular trial costs. ahajrnls.org/4vEq8mk
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#ResearchLetter: Dysregulated T-cell-mediated immunity underlies progression of arrhythmogenic right ventricular cardiomyopathy.ahajrnls.org/3ROmB6t
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