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Exercise Metabolic Memory Halts Pathological Cardiac Hypertrophy via PDK4.

Cankun Zheng1, Xiaoxia Huang2, Xinnan Wei1

  • 1Department of Cardiology, State Key Laboratory of Multi-Organ Injury Prevention and Treatment, Guangdong Provincial Key Laboratory of Cardiac Function and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou, China (C.Z., X.W., C.L., L.C., M.L., R.Z., M.H., Z.L., R.L., J.L., Q.W., H.L., Y.L.).

Circulation Research
|April 20, 2026
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Summary
This summary is machine-generated.

Exercise preconditioning creates a metabolic memory in the heart by suppressing Pdk4 via RNA methylation. This mechanism enhances glucose metabolism and produces protective metabolites, preventing pathological cardiac hypertrophy and heart failure.

Keywords:
RNA methylationarachidonic acidexercisefibrosisglucose

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Area of Science:

  • Cardiovascular Biology
  • Metabolic Regulation
  • Epigenetics

Background:

  • Pathological cardiac hypertrophy, a precursor to heart failure, is closely linked to impaired glucose metabolism.
  • Exercise enhances myocardial glucose utilization, but its long-term effects on metabolic reprogramming and prevention of cardiac hypertrophy are not fully understood.
  • This study investigates the sustained metabolic memory induced by exercise-induced hypertrophic preconditioning (EHP) and its cardioprotective mechanisms, focusing on RNA methylation and arachidonic acid metabolism.

Purpose of the Study:

  • To elucidate the mechanisms of sustained metabolic memory induced by EHP.
  • To understand the role of RNA methylation and arachidonic acid metabolism in EHP-mediated cardioprotection.
  • To explore the therapeutic potential of targeting the PDK4-arachidonic acid metabolites axis.

Main Methods:

  • Positron emission tomography/computed tomography for cardiac glucose uptake assessment.
  • Bulk RNA sequencing for myocardial gene expression profiling.
  • Genetic manipulation of Pdk4 (pyruvate dehydrogenase kinase 4) and pressure overload induction via transverse aortic constriction.
  • Analysis of RNA methylation, metabolomics, and molecular pathways.

Main Results:

  • EHP induced sustained myocardial glucose preference via METTL3-dependent m6A RNA methylation, suppressing Pdk4.
  • Pdk4 deletion improved cardiac function and reduced fibrosis under pressure overload, while Pdk4 overexpression abolished EHP's cardioprotection.
  • Arachidonic acid metabolites (5-KETE, 12-keto-LTB4, 20-hydroxy-LTB4) were identified as novel inhibitors of hypertrophy and fibrosis by targeting the ERK2/MAPK1 pathway.

Conclusions:

  • EHP establishes metabolic memory by suppressing Pdk4 through RNA methylation, altering arachidonic acid metabolism and generating protective lipid mediators.
  • Targeting the PDK4-arachidonic acid metabolites axis offers therapeutic potential for mitigating pathological cardiac remodeling and heart failure.