Autophagy Inhibition Contributes to ROS-Producing NLRP3-Dependent Inflammasome Activation and Cytokine Secretion in High Glucose-Induced Macrophages | Zendy

Jiezhi Dai | Zendy; Xiaotian Zhang | Zendy; Li Li | Zendy; Hua Chen | Zendy; Yimin Chai | Zendy

Open Access

Autophagy Inhibition Contributes to ROS-Producing NLRP3-Dependent Inflammasome Activation and Cytokine Secretion in High Glucose-Induced Macrophages

Author(s) -

Jiezhi Dai,

Xiaotian Zhang,

Li Li,

Hua Chen,

Yimin Chai

Publication year - 2017

Publication title -

cellular physiology and biochemistry

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.486

H-Index - 87

eISSN - 1421-9778

pISSN - 1015-8987

DOI - 10.1159/000480367

Subject(s) - inflammasome , autophagy , secretion , reactive oxygen species , inflammation , microbiology and biotechnology , cytokine , western blot , proinflammatory cytokine , chemistry , biology , apoptosis , immunology , biochemistry , gene

Type 2 diabetes is a persistent inflammatory response that impairs the healing process. We hypothesized that stimulation with high glucose following a pro-inflammatory signal would lead to autophagy inhibition, reactive oxygen species (ROS) production and eventually to the activation of the Nod-like receptor protein (NLRP) -3.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.

Having issues? You can contact us here

Accelerating Research