¹H NMR-Based Analysis of Serum Metabolites in Monocrotaline-Induced Pulmonary Arterial Hypertensive Rats

Figure 5

Metabolic abnormality may be a fundamental mechanism of the uncontrolled proliferative and antiapoptotic pulmonary artery smooth muscle cells in the pathogenesis of PAH. (a) Pathway enrichment analysis for determining which pathways are more likely to be involved in the PAH development. (b) Change of metabolite levels during progression of PAH. (c) Hypothetical pathways for choline, betaine, methionine, and energy metabolism dysfunction in PAH. Increased levels of choline and betaine could cause energy metabolism abnormality by affecting mitochondrial function. In PAH, PASMCs proliferation maximizes the usage of methionine for protein synthesis which might reduce the methionine level (choline dehydrogenase: CHDH; methylene tetrahydrofolate dehydrogenase: MTHFD), although methionine is the metabolic production of betaine.

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