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Updated: Jan 22, 2026

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
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Oxymatrine Alleviates Atherosclerosis by Regulating Macrophage Senescence via the SIRT1-P53 Signaling Pathway

Jun Xiang1,2,3, Sheng-Quan Wang4,5, Guang-Qiong Zhang1,2,3

  • 1The High Efficacy Application of Natural Medicinal Resources Engineering Center of Guizhou Province, Guizhou Medical University, Guiyang, Guizhou, China.

Phytotherapy Research : PTR
|January 20, 2026
PubMed

Insights

Oxymatrine (OMT) effectively treats atherosclerosis by inhibiting macrophage senescence. It stabilizes SIRT1, promoting P53 degradation to reduce foam cell formation and improve cardiovascular health.

Area of Science:

  • Cardiovascular Research
  • Cellular Biology
  • Pharmacology

Background:

  • Macrophage senescence is a key risk factor in atherosclerosis (AS) development.
  • Oxymatrine (OMT) shows promise in mitigating cellular senescence.

Purpose of the Study:

  • To investigate OMT's therapeutic effects on AS progression.
  • To elucidate the underlying molecular mechanisms of OMT action.

Main Methods:

  • In vivo (ApoE-/- mice) and in vitro (oxLDL-induced macrophages) models were utilized.
  • Network pharmacology, gene silencing, molecular docking, CETSA, and DARTS assays were employed.
  • SIRT1 and P53 pathways were specifically targeted for mechanistic investigation.

Main Results:

  • OMT significantly inhibited macrophage senescence and improved AS progression.
  • OMT directly binds to and stabilizes SIRT1 protein.
  • OMT enhances SIRT1-mediated deacetylation and degradation of P53.

Conclusions:

  • OMT demonstrates potent anti-atherosclerotic effects by targeting the SIRT1/P53 pathway.
  • OMT delays macrophage senescence and foam cell formation, offering a promising therapeutic strategy for AS.
Keywords:
atherosclerosischolesterol effluxfoam cellsmacrophage senescenceoxymatrinesirtuin 1

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