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Supplementing with the amino acid homoarginine reduced atherosclerosis in mice by modulating T-cell function. This novel mechanism involves altering T-cell cytoskeleton, inhibiting proliferation and migration, offering protection against cardiovascular disease.

Keywords:
amino acidatherosclerosisbiomarkercardiovascular diseasehomoarginine

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Area of Science:

  • Cardiovascular Research
  • Immunology
  • Amino Acid Metabolism

Background:

  • Amino acid metabolism plays a key role in inflammation during atherosclerosis.
  • High levels of the endogenous amino acid homoarginine are linked to better cardiovascular outcomes.
  • The precise mechanisms behind homoarginine's protective effects are not fully understood.

Purpose of the Study:

  • To investigate the impact of homoarginine supplementation on atherosclerotic plaque development.
  • To explore the specific effects of homoarginine on inflammation and T-cell responses in atherosclerosis.

Main Methods:

  • Female ApoE-deficient mice were supplemented with homoarginine and fed a Western-type diet.
  • Immunohistochemistry, flow cytometry, and mass spectrometry-based proteomics were employed.
  • In vitro assays assessed T-cell proliferation, migration, and cytoskeleton organization.

Main Results:

  • Homoarginine supplementation significantly increased circulating levels and reduced atherosclerosis in mice.
  • A decrease in CD3+ T cells, particularly CD4+ T cells, was observed in atherosclerotic lesions.
  • Homoarginine modulated the T-cell actin cytoskeleton, inhibited proliferation, and impaired T-cell migration.

Conclusions:

  • Homoarginine reduces atherosclerosis by modulating T-cell cytoskeleton and function.
  • This study reveals a novel mechanism for homoarginine's atheroprotective effects.
  • Findings provide a molecular basis for homoarginine's benefits in atherosclerotic cardiovascular disease.