In adult IBD, SQOR is markedly downregulated and independent of inflammation severity, suggesting an intrinsic risk factor; in UC models, SQOR loss enhances Drp1 activity, suppresses PGC1α, and disrupts the barrier. In CRC, SQOR is generally downregulated (H2S accumulation ETC., activation). However, Dawoud et al. reported early upregulation is protective, whereas late downregulation promotes metastasis, proposing the “respiratory shield” hypothesis. Here, PPARGC1A is linked to colorectal carcinoma.