Evidence map›Paper›PMID 35510944›Full record

ArticleThe Journal of cell biology2022

STING controls energy stress-induced autophagy and energy metabolism via STX17.

Yueguang Rong, Shen Zhang, Nilay Nandi, Zhe Wu, Linsen Li, Yang Liu, Yuehan Wei, Yuan Zhao, Weigang Yuan, Chuchu Zhou and 9 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of cell biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.6field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

42 citing papers in PubMed, 56 citations in OpenAlex.

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  9. AgJournal of nanobiotechnology · 2026
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  20. Molecular mechanism on autophagy associated cardiovascular dysfunction inFrontiers in cell and developmental biology · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

19 authors at 4 institutions in 2 countries.

Yueguang Rong *Department of Pathogen Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, China.
Shen Zhang *Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0003-4682-4470
Nilay Nandi *Department of Neuroscience and Department of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX.
Zhe Wu *Department of Pathogen Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, China.ORCID 0000-0003-3474-8466
Linsen LiKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yang LiuCenter for Autophagy Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX.
Yuehan WeiDepartment of Nephrology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yuan ZhaoDepartment of Pathogen Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, China.
Weigang YuanDepartment of Pathogen Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, China.
Chuchu ZhouDepartment of Pathogen Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, China.
Guanghua XiaoQuantitative Biomedical Research Center, Department of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, TX.
Beth LevineCenter for Autophagy Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX.
Nan YanDepartment of Immunology, University of Texas Southwestern Medical Center, Dallas, TX.ORCID 0000-0002-0637-3989
Shan MouDepartment of Nephrology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Liufu DengDepartment of Immunology and Microbiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Zaiming TangKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiaoxia LiuKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0002-1333-9068
Helmut KramerDepartment of Neuroscience and Department of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX.ORCID 0000-0002-1167-2676
Qing ZhongKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0001-6979-955X
Shanghai Jiao Tong University · CNHuazhong University of Science and Technology · CNThe University of Texas Southwestern Medical Center · USHoward Hughes Medical Institute · US

Funding

MOLECULAR ANALYSIS OF THE BOSS TRANSMEMBRANE LIGANDR01EY010199 · NEI · UT SOUTHWESTERN MEDICAL CENTER · PI Helmut J Kramer · 1994 to 2026
$9.7M
Laser Scanning Confocal for UT Southwestern Live Cell Imaging FacilityS10OD021684 · OD · UT SOUTHWESTERN MEDICAL CENTER · PI LUBY-PHELPS, KATHERINE J · 2016 to 2016
$455k
Ministry of Science and Technology 2019YFA0508602National Natural Science Foundation of China 91754205NEI NIH HHS R01 EY010199NIH HHS S10 OD021684Program of Shanghai Subject Chief Scientist 19XD1402200Shanghai Collaborative Innovation Center of Cellular Homeostasis Regulation and Human DiseasesShanghai Science and Technology Commission 20JC1410100
6 · The paper itself

Abstract

The stimulator of interferon genes (STING) plays a critical role in innate immunity. Emerging evidence suggests that STING is important for DNA or cGAMP-induced non-canonical autophagy, which is independent of a large part of canonical autophagy machineries. Here, we report that, in the absence of STING, energy stress-induced autophagy is upregulated rather than downregulated. Depletion of STING in Drosophila fat cells enhances basal- and starvation-induced autophagic flux. During acute exercise, STING knockout mice show increased autophagy flux, exercise endurance, and altered glucose metabolism. Mechanistically, these observations could be explained by the STING-STX17 interaction. STING physically interacts with STX17, a SNARE that is essential for autophagosome biogenesis and autophagosome-lysosome fusion. Energy crisis and TBK1-mediated phosphorylation both disrupt the STING-STX17 interaction, allow different pools of STX17 to translocate to phagophores and mature autophagosomes, and promote autophagic flux. Taken together, we demonstrate a heretofore unexpected function of STING in energy stress-induced autophagy through spatial regulation of autophagic SNARE STX17.

Indexed as

AutophagyEnergy MetabolismLysosomesMembrane ProteinsQa-SNARE ProteinsAnimalsAutophagosomesDrosophilaMiceMice, KnockoutPhysical Conditioning, AnimalSTING ProteinMembrane ProteinsQa-SNARE ProteinsSting1 protein, mouseSTING ProteinStx17 protein, mouse

Identifiers

PMID35510944
PMCPMC9082627
OpenAlexW4228997735

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.