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September 10, 2025European Heart Journal Supplements

Accelerated adverse cardiac remodeling in a model of TET2 mutation-driven clonal hematopoiesis is ameliorated by IFNa treatment by modulating the monocyte response

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Authors

LYLaura I. YousifLKLucia KimAPAriel H. Polizio

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Overview

Observational analysis shows IFNα improves cardiac function post-myocardial infarction in TET2 mutation-driven clonal hematopoiesis, indicating a shift in monocyte response.

Key Points

  • Cardiac function significantly declined in TET2-deficient mice compared to wild type after myocardial infarction, indicating adverse remodeling.
  • IFNα treatment significantly prevented the decline in left ventricular ejection fraction in TET2-deficient mice, demonstrating cardioprotective effects.
  • Treatment with IFNα led to a significant decrease in lymphocyte and neutrophil expansion while increasing anti-inflammatory monocytes.
  • Reduced myocardial inflammation after IFNα treatment was observed, suggesting modulation of IL-1β expression as a mechanism for cardioprotection.

Cite This Study

Yousif et al. (2025) studied this question.

synapsesocial.com/papers/68c1a5e554b1d3bfb60df207https://doi.org/10.1093/eurheartjsupp/suaf083.228
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Inhibiting the cGAS‐STING pathway in myeloid cells effectively improves myocardial healing related to TET2 deficiency‐induced DNA damage response2024
  2. 2Modeling cardioinflammatory TET2 CHIP in engineered cardiac ventricular tissue reveals therapeutics for disease resolution2025
  3. 3Perturbation of iNKT differentiation during clonal hematopoiesis from rewiring of inflammation and lipid presentation2025
  4. 4Response to Immune Checkpoint Blockade is Enhanced in the Presence of Hematopoietic TET2 Inactivation2025
  5. 5TET2 mutations drive cell-autonomous type I interferon production and selective advantage through TRIM4 silencing2025