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Autophagy Alteration in ApoA-I Related Systemic Amyloidosis



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Giudice, Rita Del and Imbimbo, Paola and Pietrocola, Federico and Martins, Isabelle and De Palma, Fatima Domenica Elisa and Bravo San Pedro, José Manuel and Kroemer, Guido and Maiuri, Maria Chiara and Monti, Daria Maria (2022) Autophagy Alteration in ApoA-I Related Systemic Amyloidosis. International Journal of Molecular Sciences, 23 (7). p. 3498. ISSN 1422-0067

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Official URL: https://doi.org/10.3390/ijms23073498


Amyloidoses are characterized by the accumulation and aggregation of misfolded proteins into fibrils in different organs, leading to cell death and consequent organ dysfunction. The specific substitution of Leu 75 for Pro in Apolipoprotein A-I protein sequence (ApoA-I; L75P-ApoA-I) results in late onset amyloidosis, where deposition of extracellular protein aggregates damages the normal functions of the liver. In this work, we describe that the autophagic process is inhibited in the presence of the L75P-ApoA-I amyloidogenic variant in stably transfected human hepatocyte carcinoma cells. The L75P-ApoA-I amyloidogenic variant alters the redox status of the cells, resulting into excessive mitochondrial stress and consequent cell death. Moreover, L75P-ApoA-I induces an impairment of the autophagic flux. Pharmacological induction of autophagy or transfection-enforced overexpression of the pro-autophagic transcription factor EB (TFEB) restores proficient proteostasis and reduces oxidative stress in these experimental settings, suggesting that pharmacological stimulation of autophagy could be a promising target to alleviate ApoA-I amyloidosis.

Item Type:Article
Uncontrolled Keywords:amyloidosis; autophagy; apoptosis; apolipoprotein A-I
Subjects:Medical sciences > Medicine > Gastroenterology and Hepatology
ID Code:73368
Deposited On:07 Jul 2022 14:52
Last Modified:08 Jul 2022 07:34

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