Evidence map›Paper›PMID 39349483›Full record

ArticleNPJ biofilms and microbiomes2024

Stress triggers gut dysbiosis via CRH-CRHR1-mitochondria pathway.

Yiming Zhang, Xiaoang Li, Siqi Lu, Huaizhu Guo, Zhuangyi Zhang, Haonan Zheng, Cunzheng Zhang, Jindong Zhang, Kun Wang, Fei Pei and 1 more

Abstract read
In one paragraph

Article in NPJ biofilms and microbiomes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

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  10. Neuropeptides and the Autonomic Nervous System in Prader-Willi Syndrome.International journal of molecular sciences · 2025
    Review
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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

11 authors.

Yiming Zhang *Department of Gastroenterology, Peking University Third Hospital, Haidian District, Beijing, China.
Xiaoang Li *Department of Gastroenterology, Peking University Third Hospital, Haidian District, Beijing, China.
Siqi LuDepartment of Gastroenterology, Peking University Third Hospital, Haidian District, Beijing, China.
Huaizhu GuoDepartment of Gastroenterology, Peking University Third Hospital, Haidian District, Beijing, China.
Zhuangyi ZhangDepartment of Gastroenterology, Peking University Third Hospital, Haidian District, Beijing, China.
Haonan ZhengDepartment of Gastroenterology, Peking University Third Hospital, Haidian District, Beijing, China.
Cunzheng ZhangDepartment of Gastroenterology, Peking University Third Hospital, Haidian District, Beijing, China.
Jindong ZhangDepartment of Gastroenterology, Peking University Third Hospital, Haidian District, Beijing, China.
Kun WangDepartment of Gastroenterology, Peking University Third Hospital, Haidian District, Beijing, China.
Fei PeiDepartment of Pathology, Peking University Third Hospital, Peking University School of Basic Medical Sciences, Beijing, China.
Liping DuanDepartment of Gastroenterology, Peking University Third Hospital, Haidian District, Beijing, China. duanlp@bjmu.edu.cn.

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82170557National Natural Science Foundation of China (National Science Foundation of China) 82470578
6 · The paper itself

Abstract

Stress can lead to gut dysbiosis in brain-gut axis disordered diseases as irritable bowel syndrome (IBS), yet the mechanisms how stress transfer from the brain to the gut and disrupt gut microbiota remain elusive. Here we describe a stress-responsive brain-to-gut axis which impairs colonocytes' mitochondria to trigger gut dysbiosis. Patients with IBS exhibit significantly increased facultative anaerobes and decreased obligate anaerobes, related to increased serum corticotropin-releasing hormone (CRH) level and defected colonocytes' mitochondria ultrastructure. Mice exposed to acute stress experienced enhanced CRH-CRH receptor type 1 (CRHR1) signaling, which impaired mitochondria and epithelium hypoxia in the colon, subsequently triggered gut dysbiosis. Antagonizing CRHR1 expression to inhibit cAMP/Ras/MAPK signaling or activating mitochondria respiration conferred resilience against stress-induced mitochondria damaging and epithelium hypoxia impairment, ultimately improving gut dysbiosis. These results suggest that the CRH-CRHR1-mitochondria pathway plays a pivotal role in stress-induced gut dysbiosis that could be therapeutically targeted for stress-induced gastrointestinal diseases. Yiming Zhang et.al report that psychological stress activated Corticotropin-releasing hormone (CRH)-CRH receptor type 1 (CRHR1)-mitochondria pathway to trigger gut dysbiosis and reveal CRHR1 upregulation damages mitochondria via cAMP/Ras/MAPK signaling in colonocytes.

Indexed as

Corticotropin-Releasing HormoneDysbiosisGastrointestinal MicrobiomeMitochondriaReceptors, Corticotropin-Releasing HormoneAnimalsBrain-Gut AxisColonCRF Receptor, Type 1HumansIrritable Bowel SyndromeMiceSignal TransductionStress, PsychologicalCorticotropin-Releasing HormoneCRF Receptor, Type 1Receptors, Corticotropin-Releasing Hormone

Identifiers

PMID39349483
PMCPMC11442948

What OpenQuestion holds

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Registered trials

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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.