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Figure 3 | Fibrogenesis & Tissue Repair

Figure 3

From: Lipid mediators in diabetic nephropathy

Figure 3

Implications of antidyslipidemic drugs on the antifibrotic-miRs in the protective measures of DN. Altered microRNA expression, as a result of a deregulated lipid metabolism, inflammation, oxidative stress, high blood pressure, proteinuria, and high blood glucose could cause DN by activating transforming growth factor β (TGFβ) signaling. An elevated DPP-4 level, BMP signaling, and claudin-1 could also be associated with DN. Atorvastatin improves cardiovascular functions by elevating miR-let-7i. miR-let-7i is associated with inhibiting TGFβ signaling. Farnesoid X receptor (FXR) is known to activate miR-29a, reducing DPP-4 and the associated renal fibrosis. Statins also elevate SIRT1 by inhibiting miR-34a. SIRT1 inhibits claudin-1 and associated renal fibrosis.

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