Patients with chronic kidney disease CKD have a higher risk of cardiovascular diseases and suffer from accelerated atherosclerosis. CKD patients are permanently exposed to uremic toxins, making them good candidates as pathogenic agents. Uremic toxins derived from tryptophan are endogenous ligands of the transcription factor aryl hydrocarbon receptor AhR.
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Similar to many RNA-binding proteins, TDP expression is tightly regulated through an autoregulatory negative feedback loop. Cell function and survival depend on the strict control of TDP protein levels. Several observations argue for a pathogenic role of elevated TDP levels in these disorders. Modulation of the cycle of TDP production might therefore provide a new therapeutic strategy.
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