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In cases where blood vessels malfunction, like in DR, FSP1 may play a role in controlling the growth of extra blood vessels and the formation of tough scar tissue by communicating with growth factors and the cell surface receptors, which in turn affects how the extracellular matrix changes and the series of events that lead to new blood vessel formation

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Some scholars have used the synoviocyte mitochondrial gene encoding NADH dehydrogenase 1 as an entry point in order to study the mutation level of synoviocyte mtDNA in rheumatoid arthritis, and have found that the number of mutations in RA synoviocyte mtDNA is approximately twice as high as that of the OA group, and that RA fibroblasts are expressed at a mutation load of 2.3 amino acid changes per thousand base pairs, whereas in tissues, there are 2.3 changes per 2.5 amino acid changes per thousand base pairs