Cathepsin B contributes to autophagy-related 7 (Atg7)-induced nod-like receptor 3 (NLRP3)-dependent proinflammatory response and aggravates lipotoxicity in rat insulinoma cell line

58Citations
Citations of this article
35Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

Background: Previous studies show that autophagy deficiency leads to inflammasome activation. Results: Excessive autophagy activation induces a proinflammatory response. Conclusion: Our findings provide new insights into the release mechanisms of proinflammatory cytokines regulated by autophagy. Significance: That autophagy may play a deleterious role in pathogenesis in T2D is a novel finding. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.

Cite

CITATION STYLE

APA

Li, S., Du, L., Zhang, L., Hu, Y., Xia, W., Wu, J., … Yang, S. (2013). Cathepsin B contributes to autophagy-related 7 (Atg7)-induced nod-like receptor 3 (NLRP3)-dependent proinflammatory response and aggravates lipotoxicity in rat insulinoma cell line. Journal of Biological Chemistry, 288(42), 30094–30104. https://doi.org/10.1074/jbc.M113.494286

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free