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Mechanical Stimulation-induced Calcium Wave Propagation in Cell Monolayers: The Example of Bovine Corneal Endothelial Cells
Published on: July 16, 2013
cGAS-STING and PANoptosis: Interplay, Underlying Mechanisms, and Therapeutic Targets
Yumin Wang1, Jinxia Chen2, Wenxin Feng3
1Department of Respiratory and Critical Care Medicine, Aerospace Center Hospital, Peking University Aerospace School of Clinical Medicine, Beijing, People's Republic of China.
The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway drives PANoptosis, a programmed cell death pathway, in various diseases. Targeting this crosstalk offers new therapeutic strategies for inflammatory conditions.
Area of Science:
- Innate immunity
- Cell death pathways
- DNA sensing mechanisms
Background:
- The cGAS-STING pathway detects cytosolic DNA, initiating immune responses.
- Dysregulated cGAS-STING signaling is implicated in autoimmune and inflammatory diseases.
- PANoptosis integrates pyroptosis, apoptosis, and necroptosis, contributing to pathogenesis.
Purpose of the Study:
- To propose a framework where cGAS-STING activation drives PANoptosis.
- To explore the crosstalk between cGAS-STING and PANoptosis in disease.
- To review therapeutic strategies targeting this interface.
Main Methods:
- Review of existing literature on cGAS-STING and PANoptosis.
- Analysis of molecular mechanisms linking these pathways.
- Examination of pathophysiological consequences and therapeutic interventions.
Main Results:
- cGAS-STING activation acts as an upstream driver of PANoptosis.
- This crosstalk involves cytosolic DNA sensing, ZBP1-PANoptosome assembly, and inflammatory cell death.
- Dysregulation contributes to various inflammatory and autoimmune disorders.
Conclusions:
- The cGAS-STING-PANoptosis axis is a key pathogenic mechanism.
- Targeting this interface presents promising therapeutic opportunities for inflammatory diseases.
- Nanomedicine offers solutions for targeted STING agonist delivery, minimizing toxicity.
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