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and NETs, in turn, is a known trigger for coagulation and blood vessel occlusion [359], and also involve significant erythrocyte pathologies, specifically related to rheology and oxygen carrying capacity and ultimately resulting in ischemia-reperfusion injury [352]

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In cells, homocysteine is metabolized in three ways :[ref] It can be remethylated to form methionine (requires folate, MTHFR, and vitamin B12, MTR gene or needs betaine, interacting with BHMT and PEMT genes) Can be converted to cysteine (CBS gene, serine and B6 as a cofactor), which is used in the synthesis of glutathione It can be converted to homocysteine thiolactone, which can be a problem at higher levels Lets dig into each of these pathways further: Methylation Cycle: Homocysteine, Methionine, SAMe, and SAH Homocysteine is maintained at a relatively constant level by several mechanisms in the methionine cycle

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S3 and Table S1a