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[5] This reversal is politically driven

identified that histone methyltransferase G9a/chromobox homolog 5 (CBX5)/methylated lysine 9 residue on histone 3 (H3K9me) were key regulators of fibroblast activation, and determined that by participating in the CBX5/G9a pathway, TGF and increased matrix stiffness effectively inhibited PGC1 expression in lung fibroblasts (Ligresti et al., 2019)

Mechanistically, it can dampen the pro-inflammatory response by decreasing the transcription of pro-inflammatory cytokines through direct DNA binding to Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-B) (Wang and He, 2022)

Should member schools choose, the slides may be downloaded and incorporated into their drug-testing education presentations