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Fig. 2 | Molecular Medicine

Fig. 2

From: Autosomal dominant polycystic kidney disease and pioglitazone for its therapy: a comprehensive review with an emphasis on the molecular pathogenesis and pharmacological aspects

Fig. 2

Pictorial representation of the role of intracellular calcium in the pathophysiology of ADPKD. ADPKD: Autosomal dominant polycystic kidney disease; PI3K: Phosphatidylinositol-3-kinase. In a normal kidney epithelial cell, there is an increased level of intracellular calcium due to the proper functioning of polycystin-2 at the basolateral membrane and endoplasmic reticulum (not shown in the figure) along with other calcium ion channels. Increased calcium leads to the activation of PI3K that further activates the Akt. Akt leads to the inhibition of the proliferative factor; B-Raf and therefore abate the activation of other factors of Ras/Raf/MEK/ERK pathway (shown by the dashed line). In a renal epithelial cell with mutated polycystin-2, there is a low intracellular calcium level due to which B-Raf cannot get inhibited by the decreased formation of Akt that consequently leads to unabated cell proliferation (Mitobe et al. 2010; Li et al. 2016)

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