COL1A1 and chronic kidney disease: For example, the accumulation of TMAO levels in the body promotes renal fibrosis, inflammation, and atherosclerosis, thereby accelerating the progression of CKD (166, 167); high betaine levels may lead to abnormal methylation of profibrotic genes (such as TGF-β and COL1A1), promoting renal interstitial fibrosis (168); and methylation cycle disorders in patients with CKD lead to homocysteine accumulation, whereas abnormal betaine metabolism may exacerbate reactive oxygen species production, promoting renal tubular damage (169).