Lanthionine and inflammation: an intriguing link in the context of vascular calcification in chronic kidney disease

Chronic kidney disease (CKD) is expected to be the 5th cause of death globally by 2040. Cardiovascular events represent an important cause of morbidity and mortality for these patients, with a cardiovascular risk about ten times higher than healthy controls. Vascular calcification (VC), an abnormal accumulation of calcium and phosphate in blood vessel walls, contribute to the pathogenesis of cardiovascular events in CKD, in addition to traditional risk factors like obesity, hypertension and diabetes. Several alterations of sulfur amino acids have been reported in CKD, including homocysteine and its precursor, S-adenosylhomocysteine, which are both listed in the uremic toxins group. Homocysteine is also considered a cardiovascular risk factor. Additional sulfur compounds may be interesting in this respect, including lanthionine, a non-proteinogenic sulfur amino acid and a prospective uremic toxin thought to be involved in the pathogenesis of VC. Main scope of the present review is to assess the current knowledge on the role of lanthionine as a uremic toxin, and its potential involvement in the development of cardiovascular lesions in CKD.