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October 9, 2025Circulation Research

Abstract Wed080: Cardiac-specific mTORC1 Suppression Protects Against the Development of Heart Failure with Preserved Ejection Fraction

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Authors

KKKamil KobakCKCatherine KingWZWeronika Zarzycka

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Overview

Cardiac-specific mTORC1 suppression prevents cardiac hypertrophy and dysfunction in HFpEF, highlighting its therapeutic potential.

Key Points

  • Suppression of mTORC1 protects against heart failure with preserved ejection fraction, maintaining normal cardiac function.
  • MCM-Raptor het KO mice did not show cardiac hypertrophy or diastolic dysfunction after 15 weeks of stress, unlike controls.
  • Mechanisms include a reduction in protein synthesis and enhanced autophagy, linking mTORC1 hyperactivation to disease progression.
  • Disrupted proteostasis and mTORC1 activation are key contributors to HFpEF pathogenesis, indicating a potential therapeutic target.

Cite This Study

Kobak et al. (2025) studied this question.

synapsesocial.com/papers/68e77f09d1c187e1c108fbe3https://doi.org/10.1161/res.137.suppl_1.wed080
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Also Consider

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

  1. 1Abstract Wed081: Cardiomyocyte METTL3 Protects Against Heart Failure with Preserved Ejection Fraction2025
  2. 2Abstract Wed091: Biomechanical and Transcriptomic Remodeling of the Heart in Heart Failure with Preserved Ejection Fraction2025
  3. 3Abstract Wed077: The role of senescence in HFpEF induced by cardiometabolic syndrome2025
  4. 4Abstract Wed078: Post-transcriptional Regulation of Adrenal-Heart Crosstalk in Heart Failure with Preserved Ejection Fraction2025
  5. 5Abstract Fri112: Mitochondrial Maladaptation at the Crossroads of Heart Failure: A Tale of Two Phenotypes2025