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ACBP/DBI protein neutralization confers autophagy-dependent organ protection through inhibition of cell loss, inflammation, and fibrosis

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Significance Pharmacological induction of autophagy usually involves small molecules targeting intracellular signaling cascades. Here, Motiño et al. demonstrate that monoclonal antibody–mediated neutralization of an extracellular inhibitor of autophagy, acyl-coenzyme A… Click to show full abstract

Significance Pharmacological induction of autophagy usually involves small molecules targeting intracellular signaling cascades. Here, Motiño et al. demonstrate that monoclonal antibody–mediated neutralization of an extracellular inhibitor of autophagy, acyl-coenzyme A binding protein (ACBP)/diazepam-binding inhibitor (DBI), stimulates cytoprotective autophagy, hence inhibiting cell loss, inflammation, and fibrosis in various disease models affecting liver, lung, and myocardium. Extracellular ACBP/DBI acts as an autophagy checkpoint on GABAA receptors, hence offering a target for a new class of autophagy checkpoint inhibitors.

Keywords: cell loss; dbi; loss inflammation; inflammation fibrosis; acbp dbi; autophagy

Journal Title: Proceedings of the National Academy of Sciences of the United States of America
Year Published: 2022

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