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Related Concept Videos

Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
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Cellular Adaptation II: Hypertrophy

Hypertrophy is the increase in the size of individual cells, resulting in the enlargement of a tissue or organ. Unlike hyperplasia, which involves an increase in cell number, hypertrophy is characterized by an increase in cell volume. This process often occurs in response to higher functional demand or hormonal stimulation, leading to the production of more structural proteins and organelles, thereby enhancing the cells' work capacity.There are two primary types of hypertrophy: physiological...
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Overview of Carbohydrate Metabolism

Carbohydrate metabolism is a fundamental biochemical process that ensures a constant supply of energy to living cells. The most important carbohydrate is glucose, which can be broken down via glycolysis to enter into the Krebs cycle and eventually lead to the production of ATP through oxidative phosphorylation.
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Managing cardiomyopathy involves addressing underlying or precipitating causes, treating heart failure with medications, and implementing dietary changes and a balanced exercise and rest regimen.Lifestyle ModificationsCardiomyopathy patients should adopt a low-sodium diet to reduce fluid retention and manage heart failure. A personalized exercise and rest plan helps maintain physical fitness without overstraining the heart. Avoiding alcohol and tobacco is essential to prevent further damage to...

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Related Experiment Video

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Mouse Electroacupuncture Fixation Device Fabrication for Electroacupuncture Pretreatment in Diabetic Cardiomyopathy Mouse Model
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Sam68 Exacerbates Pathologic Cardiac Hypertrophy by Suppressing Cardiomyocyte Glucose Oxidation.

Junqing An1, Chaoshan Han1, Ying Jiang2

  • 1Department of Pharmacology, Homeostatic Medicine Institute, School of Medicine, Southern University of Science and Technology, Shenzhen, Guangdong, China (J.A., C.H., C.W., J.H., J.N., Y.C., Y.F., G.Q.).

Circulation
|May 22, 2026
PubMed
Summary

Sam68 protein drives heart failure by inhibiting glucose oxidation. Blocking the Sam68-Src-STAT3-PDK4 pathway restores energy production and limits cardiac remodeling, offering a new therapeutic target.

Keywords:
cardiomegalyheart failurepyruvate dehydrogenase kinase 4ventricular remodeling

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Published on: November 29, 2024

Area of Science:

  • Cardiology
  • Molecular Biology
  • Metabolic Research

Background:

  • Pathologic cardiac hypertrophy involves metabolic remodeling and impaired glucose oxidation.
  • The mechanisms linking stress signaling to reduced myocardial glucose oxidation are not fully understood.
  • Sam68 (Src-associated in mitosis, 68 kDa), an RNA-binding protein, was not previously linked to cardiac metabolic control.

Purpose of the Study:

  • To investigate the role of Sam68 in cardiac hypertrophy and metabolic regulation.
  • To elucidate the molecular mechanisms by which Sam68 influences myocardial glucose metabolism.
  • To evaluate the therapeutic potential of targeting the Sam68-mediated pathway in heart failure.

Main Methods:

  • Examined Sam68 expression in human failing hearts and transcriptomic data.
  • Utilized cardiomyocyte-specific Sam68 knockout (Sam68cKO) and overexpression (Sam68OE) mouse models.
  • Employed transverse aortic constriction and angiotensin II infusion models for pressure overload.
  • Conducted RNA sequencing, metabolomics, 13C-glucose tracing, coimmunoprecipitation, and protein-protein docking.
  • Tested therapeutic interventions including a PDK4 inhibitor and a Sam68-Src interface blocker (YB-0158).

Main Results:

  • Sam68 expression was elevated in failing human and murine hypertrophic hearts.
  • Sam68 deletion attenuated hypertrophy, while overexpression aggravated it.
  • Sam68 inhibition restored glucose oxidation and improved oxidative-anaplerotic balance during pressure overload.
  • Sam68 acts as a scaffold promoting Src-dependent STAT3 phosphorylation, leading to PDK4 induction and PDH inhibition.
  • Pharmacologic inhibition of PDK4 or the Sam68-Src interface improved cardiac remodeling.

Conclusions:

  • Sam68 is a stress-activated scaffold in cardiomyocytes that promotes pathologic hypertrophy via a Src-STAT3-PDK4 pathway.
  • This pathway inhibits pyruvate dehydrogenase (PDH) activity, suppressing glucose oxidation.
  • Disrupting the Sam68 axis offers a therapeutic strategy for heart failure by restoring pyruvate oxidation and limiting remodeling.