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RESULTS TRPA1-/-ApoE-/- mice revealed a significant upsurge in atherosclerosis plaques in comparison to ApoE-/- mice after HFD treatment. Conversely, activation of TRPA1 by CIN sharply paid off atherosclerosis development. Atherosclerosis ended up being connected with a substantial change in macrophage polarization toward the M1 proinflammatory phenotype. We unearthed that inhibition of TRPA1 extremely stimulated M1 marker genetics phrase, while repressed M2 marker genes appearance. The connection between