Hye Khan

Abstract Progress has been made in our understanding of the mechanisms of endoplasmic reticulum (ER) proteostasis, ER stress and the unfolded protein response (UPR), as well as ER stress-induced autophagy, in the kidney. Experimental models have revealed that disruption of the UPR, including a protein that senses misfolded proteins (namely, inositol-requiring enzyme 1α) in mouse podocytes causes podocyte injury and albuminuria as mice age.

Compared with the DSN group, DSH rats showed elevated SBP after three weeks on a high salt diet, which continued to increase in response to this diet (Fig. 1a). HCTZ treatment significantly prevented the increase in SBP induced by the high salt diet (Fig. 1a). A renal ultrasound was performed to detect changes in the renal RI (Fig. 1b, g–i). In parallel with the alterations in SBP, the renal RI increased significantly in the DSH group (Fig. 1g) compared with the DSN group (Fig. 1h).