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Whether solid, liquid, or gas, a substance's state depends on the order and arrangement of its particles (atoms, molecules, or ions). Particles in the solid pack closely together, generally in a pattern. The particles vibrate about their fixed positions but do not move or squeeze past their neighbors. In liquids, although the particles are closely spaced, they are randomly arranged. The position of the particles are not fixed—that is, they are free to move past their neighbors to...
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Transition metals are defined as those elements that have partially filled d orbitals. As shown in Figure 1, the d-block elements in groups 3–12 are transition elements. The f-block elements, also called inner transition metals (the lanthanides and actinides), also meet this criterion because the d orbital is partially occupied before the f orbitals.
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Related Experiment Video

Updated: Feb 12, 2026

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Modeling the Transition From Decompensated to Pathological Hypertrophy.

Florencia Pascual1, Jonathan C Schisler2,3,4, Trisha J Grevengoed1

  • 1Department of Nutrition, University of North Carolina at Chapel Hill, NC.

Journal of the American Heart Association
|April 7, 2018
PubMed
Summary

Cardiac-specific inactivation of long-chain acyl-CoA synthetase 1 (ACSL1) in mice causes metabolic shifts and hypertrophy. This study reveals distinct early effects of ACSL1 reduction on cardiac substrate utilization and signaling.

Keywords:
mTORRNAseqfatty acidfibrosisfuel switchingglycolysismetabolomicsoxidation

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Area of Science:

  • Cardiovascular Biology
  • Metabolic Regulation
  • Molecular Cardiology

Background:

  • Long-chain acyl-CoA synthetases (ACSL) are crucial for fatty acid metabolism.
  • Cardiac ACSL1 inactivation shifts energy production from fatty acid oxidation to glycolysis.
  • This metabolic shift promotes mTORC1-mediated ventricular hypertrophy.

Purpose of the Study:

  • To investigate the early metabolic and transcriptional effects of impaired fatty acid oxidation in the heart.
  • To understand the development of cardiac hypertrophy following ACSL1 genetic inactivation.
  • To examine the impact on cardiac function.

Main Methods:

  • Unbiased metabolomics and gene expression analyses were employed.
  • Cardiac-specific temporal knockout of ACSL1 was performed in mice.
  • Transcriptional responses were compared at 2 and 10 weeks post-ablation.

Main Results:

  • ACSL1 ablation led to differential gene expression in cardiac metabolism, fibrosis, and hypertrophy pathways.
  • Partial ACSL1 reduction uniquely upregulated fibrosis genes, unlike complete knockout.
  • Metabolomic analysis revealed altered metabolites, which were normalized by rapamycin treatment.

Conclusions:

  • Short-term ACSL1 inactivation causes distinct metabolic and transcriptional changes compared to complete knockout.
  • This suggests heart-specific mechanistic target of rapamycin (mTOR) signaling during early substrate switching.
  • The observed hypertrophy with normal cardiac function serves as a model for studying the transition to pathological hypertrophy.