Evidence map›Paper›PMID 42406105›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026

Agmatine induces mitophagy via the PTS-I2R pathway to increase autophagic flux and attenuate sepsis-induced intestinal epithelial cell apoptosis.

He Jin, Shuangqin Yin, Yongming Li, Xiangwei Hou, Lin Qiao, Tianyin Kuang, Jing Zhou, Xue Yang, Wanting Zeng, Chao Fan and 9 more

Abstract read
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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

He JinState Key Laboratory of Trauma and Chemical Poisoning, Department of Wound Infection and Drug, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Shuangqin YinState Key Laboratory of Trauma and Chemical Poisoning, Department of Wound Infection and Drug, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Yongming LiChinese People's Liberation Army Unit 31636, Chuxiong, 675000, Yunnan, China.
Xiangwei HouChinese People's Liberation Army Unit 73049, Suzhou, 215101, Jiangsu, China.
Lin QiaoState Key Laboratory of Trauma and Chemical Poisoning, Department of Wound Infection and Drug, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Tianyin KuangState Key Laboratory of Trauma and Chemical Poisoning, Department of Wound Infection and Drug, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Jing ZhouState Key Laboratory of Trauma and Chemical Poisoning, Department of Wound Infection and Drug, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Xue YangState Key Laboratory of Trauma and Chemical Poisoning, Department of Wound Infection and Drug, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Wanting ZengState Key Laboratory of Trauma and Chemical Poisoning, Department of Wound Infection and Drug, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Chao FanDepartment of Laboratory Medicine, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Li LuoState Key Laboratory of Trauma and Chemical Poisoning, Department of Wound Infection and Drug, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Lihui WangDepartment of Gastroenterology, 926th Hospital of Joint Logistics Support Force of PLA, Kaiyuan, 661600, China.
Hongyan XiaoState Key Laboratory of Trauma and Chemical Poisoning, Department of Wound Infection and Drug, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Shengxiang AoState Key Laboratory of Trauma and Chemical Poisoning, Department of Wound Infection and Drug, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Shan SuState Key Laboratory of Trauma and Chemical Poisoning, Department of Wound Infection and Drug, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Quanwei BaoMedical Center of Trauma and War injuries, Daping Hospital, Army Medical University, Chongqing, 400042, China.
Yibin OuyangDepartment of Neurosurgery, The Second Affiliated Hospital of Hainan Medical University, Haikou, 570216, Hainan, China. 55922527@qq.com.
Huaping LiangState Key Laboratory of Trauma and Chemical Poisoning, Department of Wound Infection and Drug, Daping Hospital, Army Medical University, Chongqing, 400042, China. lianghuaping@tmmu.edu.cn.
Junyu ZhuState Key Laboratory of Trauma and Chemical Poisoning, Department of Wound Infection and Drug, Daping Hospital, Army Medical University, Chongqing, 400042, China. zjykent@tmmu.edu.cn.

Funding

General Program of Chongqing Natural Science Foundation CSTB2025NSCQ-GPX0575Joint Program on Health Science & Technology Innovation of Hainan Province WSJK2025ZD221Kunming University of Science and Technology Medical Joint Special Program KUST-9262026004YNational Natural Science Foundation of China 82202422Project funded by China Postdoctoral Science Foundation 2023M734253Special Project of Science and Technology Innovation Capacity Promotion of Army Medical University 2023XJS47Special Project of Science and Technology Innovation Capacity Promotion of Army Medical University 2025XQN09
6 · The paper itself

Abstract

backgroundThe therapeutic options for sepsis-induced intestinal injury, which drives multiple organ dysfunction and mortality, are limited, but the role of polyamine supplements remains unclear. This study aimed to elucidate the protective effect of agmatine (AGM) on sepsis-induced intestinal injury and its mitochondrial-targeted antiapoptotic mechanism in intestinal epithelial cells (IECs).

methodsWe verified the transport and subcellular localization of AGM in IECs via fluorescence assays and established in vitro and in vivo IEC apoptosis models. Functional evaluations using cell viability assays, laser confocal imaging, flow cytometry, transmission electron microscopy, and multiomics techniques were performed.

resultsAGM attenuated sepsis-induced intestinal injury, as evidenced by its ability to lower the serum levels of intestinal damage markers in septic mice, attenuate inflammatory factor production and pathological damage in the intestine, and reduce IEC apoptosis. AGM entered IECs via the polyamine transport system (PTS), but not the NMDA receptor, and inhibited IEC apoptosis induced by TNFα/CHX or TNFα/ActD. Notably, AGM exerted its antiapoptotic effect by targeting the mitochondrial imidazoline I2 receptor (I2R). Mechanistically, AGM induced mitophagy by decreasing the mitochondrial membrane potential without altering mitochondrial number or function, as ROS production, calcium ion influx, ATP generation, and oxygen consumption were unchanged. AGM also increased autophagic flux, as confirmed upon treatment with various autophagy inhibitors.

conclusionAGM alleviates sepsis-induced intestinal injury via the PTS-I2R axis by promoting mitophagy and autophagic flux to inhibit IEC apoptosis, laying a foundation for the use of AGM as a potential nutritional supplement or therapeutic agent for sepsis-induced intestinal injury.

Indexed as

AgmatineImidazoline ReceptorsSepsisAnimalsApoptosisAutophagyCell LineEpithelial CellsHumansIntestinal MucosaMaleMiceMice, Inbred C57BLMitochondriaMitophagyPolyaminesAgmatineImidazoline ReceptorsPolyaminesAgmatineApoptosisImidazoline I2 receptorMitophagyPolyamine transport systemSepsis-induced intestinal injury

Identifiers

PMID42406105

What Socratic holds

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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 Socratic graph.