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The STING1 network regulates autophagy and cell death
Ruoxi Zhang1, Rui Kang1, Daolin Tang2
1Department of Surgery, UT Southwestern Medical Center, Dallas, TX, USA.
Signal Transduction and Targeted Therapy
|June 3, 2021
Summary
The endoplasmic reticulum protein STING1 regulates immune responses and various cell death types, including apoptosis and necroptosis. Understanding STING1
Area of Science:
- Immunology and Molecular Biology
- Cellular Biology and Biochemistry
Background:
- The endoplasmic reticulum (ER) protein STING1 (Stimulator of Interferon Genes) is crucial for innate immunity, mediating responses to DNA from pathogens or host damage.
- STING1 activation triggers type I interferons (IFNs) and pro-inflammatory cytokines via transcription factor signaling.
Purpose of the Study:
- To review recent advancements in understanding STING1's regulatory mechanisms and signaling pathways in autophagy and diverse cell death processes.
- To explore the potential of STING1 as a therapeutic target in various health and disease contexts.
Main Methods:
- Literature review and synthesis of current research on STING1 signaling.
- Analysis of STING1's role in autophagy and multiple programmed cell death pathways.
Main Results:
- STING1 is increasingly recognized for its involvement beyond immunity, impacting cellular homeostasis through autophagy regulation.
- Emerging evidence highlights STING1's critical role in orchestrating various cell death modalities, including apoptosis, necroptosis, pyroptosis, ferroptosis, mitotic cell death, and immunogenic cell death (ICD).
Conclusions:
- STING1 acts as a central regulator connecting innate immunity, autophagy, and multiple cell death pathways.
- Further elucidation of STING1's complex roles may unveil novel therapeutic strategies for diseases involving inflammation and cell death.
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