- Meet the First Authors. [Journal Article]Circ Res. 2026 Aug 28; 139(6):e000767.CircR
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- Methylmalonate, a Metabolic Scar in the Diabetic Heart. [Editorial]Circ Res. 2026 Aug 28; 139(6):e329228.CircR
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- Hepatic ChREBP Drives Cardiac Remodeling via ApoM Nontranscriptional Repression. [Journal Article]Circ Res. 2026 Aug 26. [Online ahead of print]CircR
- CONCLUSIONS: This work identifies the hepatic ChREBP-SURF4-ApoM axis as a critical pathway in cardiac remodeling, and induction of hepatic ApoM secretion constitutes a new promising approach for treating cardiac remodeling and heart failure.
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- Mitophagy Facilitates Cytosolic Proteostasis to Preserve Cardiac Function. [Journal Article]
- CONCLUSIONS: Stimulation of mitophagy in cardiomyocytes facilitates removal of cytosolic protein aggregates as a mechanism to ameliorate proteotoxic cardiomyopathy.
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- Regulated HSPG Signaling Directs Epicardial Behavior to Support Cardiac Formation. [Journal Article]Circ Res. 2026 Aug 25. [Online ahead of print]CircR
- CONCLUSIONS: Our study highlights, for the first time, essential fine-tuning of HSPG-dependent signaling to modulate key processes in heart formation, offering potential insights for therapeutically targeting congenital heart disease and enhancing epicardial proregenerative behaviors.
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- FPR1-Driven Neutrophil-Endothelial Cell Axis Promotes Angiogenesis in PAOD. [Journal Article]Circ Res. 2026 Aug 21. [Online ahead of print]CircR
- CONCLUSIONS: FPR1 is a central regulator of inflammation and angiogenesis in PAOD. Biased FPR1 activation engages a neutrophil/CCL2-endothelial/HMOX1 axis to resolve inflammation and promote angiogenesis, supporting its therapeutic potential in PAOD.
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- Desmoplakin Loss Leads to PKC- and Src-Mediated Contractile Dysfunction in Cardiomyocytes. [Journal Article]
- CONCLUSIONS: Our study reveals a mechanism by which a desmosomal mutation affects cardiomyocyte function at the sarcomere level through activation of key signaling pathways that have not previously been implicated in desmoplakin cardiomyopathy.
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- Single-Molecule Imaging Reveals ERK-Dependent Spatial Translation in Cardiomyocytes. [Journal Article]Circ Res. 2026 Aug 21. [Online ahead of print]CircR
- CONCLUSIONS: Our high-resolution single-cell study demonstrates that protein translation in cardiomyocytes is dynamic and responsive to hypertrophic stimuli in an ERK-dependent manner. The localized translation mechanism allows cardiomyocytes to rapidly adapt to changing environments by preferentially translating mRNAs in the perinuclear region. These findings provide new insights into the spatial regulation of translation in cardiomyocytes and its role in cardiac hypertrophy.
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- Desmoplakin Mutations in Cardiac Fibroblasts Cause TGFβ1-Mediated Pathological Fibrogenesis in Desmoplakin Cardiomyopathy Via Beclin-1 Regulation. [Journal Article]
- CONCLUSIONS: Our data reveal that DSP deficiency in MSCs/fibroblasts leads to exaggerated fibrogenesis in DSP-cardiomyopathy by decreasing BECN1 availability for autophagy and CAV1-endocytosis. Overexpression of VIM binding domains of DSP could be a new strategy to treat pathological fibrosis.
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- Myeloid Activator Protein-1 Complex Contributes to Salt-Sensitive Hypertension. [Journal Article]Circ Res. 2026 Aug 17. [Online ahead of print]CircR
- CONCLUSIONS: These findings identify AP-1 as a key transcriptional driver linking dietary sodium, immune activation, and salt-sensitivity of blood pressure. Targeting AP-1 signaling mitigates immune-mediated renal and vascular injury, highlighting a novel mechanistic pathway and a therapeutic target for salt-sensitive hypertension.
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- Selective cGAS Inhibition Is Cardioprotective After Myocardial Infarction. [Letter]Circ Res. 2026 Aug 17. [Online ahead of print]CircR
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- Correction to: Single-Cell Atlas of Cardiac Endothelial Cell Heterogeneity in Pressure Overload. [Journal Article]Circ Res. 2026 Aug 14; 139(5):e000765.CircR
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