Figure 1 Pathogenic mechanisms and pathways in ADPKD

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This lecture was conducted during the Nephrology Unit Grand Ground by a Sub-intern under Nephrology Division, Department of Medicine in King Saud University.

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Figure 1 Pathogenic mechanisms and pathways in ADPKD Figure 1 | Pathogenic mechanisms and pathways in ADPKD. Loss of polycystin 1 (PC1) and/or polycystin 2 (PC2) activity leads to measurable biochemical changes in several cellular signalling pathways, including elevated cAMP levels and increased activation of mechanistic target of rapamycin (mTOR) complex 1, extracellular signal-regulated kinase (ERK), and Janus kinase–signal transducer and activator of transcription (JAK–STAT) signalling pathways with reductions in intracellular calcium levels and 5′-AMP-activated protein kinase (AMPK) activation. These alterations lead to subsequent cyst formation, cellular proliferation and metabolic dysregulation, including alterations in the level of arginine vasopressin (AVP). Each of the above mechanisms has been observed with loss of PC1 or PC2 function, although the relative contribution of each mechanism probably varies from patient to patient. Lanktree, M. B. & Chapman, A. B. (2017) New treatment paradigms for ADPKD: moving towards precision medicine Nat. Rev. Nephrol. doi:10.1038/nrneph.2017.127