Evidence map›Paper›PMID 38913144›Full record

ArticleInflammation2025

Non-Canonical STING-PERK Pathway Modulation of Cellular Senescence and Therapeutic Response in Sepsis-Associated Acute Kidney Injury.

Yuxin Dong, Guanghe Liu, Xiaonan Situ, Lei Xia, Tianyi Zhang, Xiangxi Zhu, Heng Jin, Yancun Liu, Songtao Shou

Abstract read
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In one paragraph

Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

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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

9 authors.

Yuxin Dong *Department of Emergency Medicine, Tianjin Medical University General Hospital, 154 Anshan Road, Heping District, Tianjin, 300052, China.
Guanghe Liu *Department of Emergency Medicine, Tianjin Medical University General Hospital, 154 Anshan Road, Heping District, Tianjin, 300052, China.
Xiaonan Situ *Department of Emergency Medicine, Tianjin Medical University General Hospital, 154 Anshan Road, Heping District, Tianjin, 300052, China.
Lei XiaDepartment of Emergency Medicine, Tianjin Medical University General Hospital, 154 Anshan Road, Heping District, Tianjin, 300052, China.
Tianyi ZhangDepartment of Emergency Medicine, Tianjin Medical University General Hospital, 154 Anshan Road, Heping District, Tianjin, 300052, China.
Xiangxi ZhuZunyi Medical University, No. 368 Jinwan Road, Jinhaian Community, Sanzao Town, Jinwan District, Zhuhai, 519041, Guangdong, China.
Heng JinDepartment of Emergency Medicine, Tianjin Medical University General Hospital, 154 Anshan Road, Heping District, Tianjin, 300052, China. hengjin@tmu.edu.cn.
Yancun LiuDepartment of Emergency Medicine, Tianjin Medical University General Hospital, 154 Anshan Road, Heping District, Tianjin, 300052, China. yancunliu@tmu.edu.cn.
Songtao ShouDepartment of Emergency Medicine, Tianjin Medical University General Hospital, 154 Anshan Road, Heping District, Tianjin, 300052, China. zyyshou@tmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Abstract-This study explored the role of the non-canonical STING-PERK signaling pathway in sepsis-associated acute kidney injury (SA-AKI). Gene expression data from the GEO database and serum STING protein levels in patients with SA-AKI were analyzed. An LPS-induced mouse model and an in vitro model using HK-2 cells were used to investigate the role of STING in SA-AKI. STING expression was suppressed using shRNA silencing technology and the STING inhibitor C176. Kidney function, inflammatory markers, apoptosis, and senescence were measured. The role of the STING-PERK pathway was investigated by silencing PERK in HK-2 cells and administering the PERK inhibitor GSK2606414. STING mRNA expression and serum STING protein levels were significantly higher in patients with SA-AKI. Suppressing STING expression improved kidney function, reduced inflammation, and inhibited apoptosis and senescence. Silencing PERK or administering GSK2606414 suppressed the inflammatory response, cell apoptosis, and senescence, suggesting that PERK is a downstream effector in the STING signaling pathway. The STING-PERK signaling pathway exacerbates cell senescence and apoptosis in SA-AKI. Inhibiting this pathway could provide potential therapeutic targets for SA-AKI treatment.

Indexed as

Acute Kidney InjuryCellular SenescenceeIF-2 KinaseMembrane ProteinsSepsisAnimalsApoptosisCell LineHumansMaleMiceMice, Inbred C57BLSignal TransductionSTING ProteinEIF2AK3 protein, humaneIF-2 KinaseMembrane ProteinsSTING1 protein, humanSting1 protein, mouseSTING Proteincell apoptosiscellular senescenceinflammationsepsis-associated acute kidney injurySTING pathway

Identifiers

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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.