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Resolving monocytes generated through TRAM deletion attenuate atherosclerosis.

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Targeting TRIF-related adaptor molecule (TRAM) reprograms inflammatory monocytes into resolving monocytes. TRAM deficiency promotes atherosclerosis regression by enhancing resolving monocyte phenotypes and intercellular communication.

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Area of Science:

  • Immunology
  • Cardiovascular Biology
  • Molecular Medicine

Background:

  • Low-grade inflammatory monocyte polarization drives atherosclerosis pathogenesis.
  • Mechanisms and therapeutic strategies for resolving monocyte polarization in atherosclerosis remain unclear.

Purpose of the Study:

  • To investigate the role of TRIF-related adaptor molecule (TRAM) in monocyte polarization.
  • To explore TRAM as a therapeutic target for atherosclerosis regression.

Main Methods:

  • In vivo and in vitro studies of TRAM-mediated monocyte polarization.
  • Analysis of signaling pathways including Src family kinase c-SRC, STAT1/STAT5, and PPARγ.
  • Assessment of peroxisome homeostasis and reactive oxygen species reduction.
  • Evaluation of TRAM-deficient mice in high-fat diet models and therapeutic transfusion studies.

Main Results:

  • TRAM mediates monocyte polarization by activating c-SRC, inducing inflammatory mediators (CCR2, SIRP-α), and suppressing resolving mediators (CD200R).
  • TRAM deficiency enhances PPARγ and Pex5, promoting peroxisome homeostasis, reducing reactive oxygen species, and establishing a resolving monocyte phenotype.
  • TRAM-deficient monocytes communicate resolving phenotypes via CD200R.
  • TRAM-deficient mice exhibit resistance to diet-induced atherosclerosis, and TRAM-deficient monocyte transfusion reduces atherosclerotic progression.

Conclusions:

  • TRAM is a key regulator of monocyte polarization in atherosclerosis.
  • Targeting TRAM can generate resolving monocytes, offering a novel therapeutic approach for atherosclerosis treatment.