Fig. 7: Beclin-1 dependent autophagy activation contributes to lipotoxicity and fibrotic responses induced by UUO. | Cell Death Discovery

Fig. 7: Beclin-1 dependent autophagy activation contributes to lipotoxicity and fibrotic responses induced by UUO.

From: Autophagy activation contributes to lipid accumulation in tubular epithelial cells during kidney fibrosis

Fig. 7: Beclin-1 dependent autophagy activation contributes to lipotoxicity and fibrotic responses induced by UUO.

In TECs from UUO-induced fibrotic kidneys, Beclin-1 is recruited to endoplasmic reticulum (ER) and initiates the biogenesis of autophagosome, which might facilitate the lipid droplets (LDs) formation induced by redundant intracellular Fatty acids (FAs), causing renal lipotoxicity and fibrotic responses; Inhibition of autophagy reduces the expression of Beclin-1, which impairs the intensity of intracellular free FAs and decreases the ectopic deposition of LDs in TECs, leading to reduction of renal lipotoxicity and prevention of the progression of kidney fibrosis

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