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Pulmonary Fibroblast Models Pathological fibrosis, an endpoint of many chronic inflammatory diseases, involves the excessive deposition of ECM by activated fibroblasts

It also interacts with the nitric-oxide pathway, which contributes to its effects on blood flow and tissue protection

If methionine intake exceeds the liver's remethylation capacity, homocysteine accumulates

Its well-defined chemical behavior supports controlled experimental conditions in biochemical analysis