Evidence map›Paper›PMID 41178622›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Type II Alveolar Epithelial Cells Promote Sepsis-Induced Immunosuppression in Alveolar Macrophages via Exosomal lncRNA Rmrp Release.

Chengxi Liu, Weixia Xuan, Song Cao, Huayun Jia, Qian Wu, Xiaowu Tan, Qijie Wang, Xiaojun Li, Lisha Ding, Yaru Xiong and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
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

18 authors.

Chengxi LiuDepartment of Anesthesiology, Anesthesiology and Pain Research Institute, the Second Affiliated Hospital, University of South China, Hengyang, Hunan, 421001, China.
Weixia XuanDepartment of Respiratory and Critical Care Medicine, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, Henan, 450003, China.
Song CaoDepartment of Pain Medicine, The Tenth Affiliated Hospital, Southern Medical University (Dongguan People's Hospital), Dongguan, Guangdong, 523000, China.
Huayun JiaBiosafety Level 3 Laboratory, Hunan Province Center for Disease Control and Prevention, Changsha, Hunan, 410005, China.
Qian WuInstitute of Human Virology, Zhongshan School of Medicine, and Key Laboratory of Tropical Disease Control of Ministry of Education, Sun Yat-sen University, Guangzhou, 510275, China.
Xiaowu TanPulmonary and Critical Care Medicine, the Second Affiliated Hospital, University of South China. Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China.
Qijie WangDepartment‌ of Infectious Disease, The Central Hospital of Shaoyang, Shaoyang, Hunan, 422000, China.
Xiaojun LiBiosafety Level 3 Laboratory, Hunan Province Center for Disease Control and Prevention, Changsha, Hunan, 410005, China.
Lisha DingBiosafety Level 3 Laboratory, Hunan Province Center for Disease Control and Prevention, Changsha, Hunan, 410005, China.
Yaru XiongBiosafety Level 3 Laboratory, Hunan Province Center for Disease Control and Prevention, Changsha, Hunan, 410005, China.
Meiyun ZhaoPulmonary and Critical Care Medicine, the Second Affiliated Hospital, University of South China. Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China.
Longcheng ZhengDepartment of Respiratory and Critical Care Medicine, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, Henan, 450003, China.
Yunzhu XiPulmonary and Critical Care Medicine, the Second Affiliated Hospital, University of South China. Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China.
Jianhua TanPulmonary and Critical Care Medicine, the Second Affiliated Hospital, University of South China. Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China.
Rong LiPulmonary and Critical Care Medicine, the Second Affiliated Hospital, University of South China. Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China.
Xulong ZhangDepartment of lmmunology, School of Basic Medical Sciences, Capital Medical University, Beijing, China.
Wenjie LiuDepartment of Anesthesiology, Anesthesiology and Pain Research Institute, the Second Affiliated Hospital, University of South China, Hengyang, Hunan, 421001, China.
Xu WuPulmonary and Critical Care Medicine, the Second Affiliated Hospital, University of South China. Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China.ORCID https://orcid.org/0000-0001-7211-5542

Funding

Beijing Natural Science Foundation 7242012Hunan Clinical Research Center for Acute and Chronic Pain 2023SK4014National Natural Science Foundation of China 82071747National Natural Science Foundation of China 82200003National Natural Science Foundation of China 82200017National Natural Science Foundation of China 82301447The Health Research Project of Hunan Provincial Health Commission 20255112The Key R&D Program of Hunan Provincial Natural Science Funds 2024JK2131The Science and Technology Innovation Program of Hunan Province 2023RC3198
6 · The paper itself

Abstract

Secondary pneumonia, a common complication of sepsis-induced immunosuppression (SII), is closely linked to alveolar macrophage (AM) dysfunction primarily due to impaired glycolytic activity. However, the underlying molecular mechanisms remain unclear. In this study, it is found that exosomal RNA component of the mitochondrial RNA processing endoribonuclease (Rmrp), derived from type II alveolar epithelial cells (AEC-IIs), drives glycolytic defects and immune tolerance in AMs following cecal ligation and puncture (CLP) sepsis. Targeted depletion of Rmrp in either AEC-IIs or AMs alleviated SII and secondary pneumonia induced by Pseudomonas aeruginosa infection 48 h post CLP. Mechanistically, Rmrp interacts with and inhibits the ubiquitination and degradation of the RNA-binding protein zinc finger protein 36 (ZFP36). This results in ZFP36 upregulation, subsequently accelerating the decay of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 (Pfkfb3) mRNA by binding to its AU-rich elements in the 3' untranslated region. The degradation of Pfkfb3 mRNA leads to impaired glycolysis and suppresses immune responses in AMs after sepsis. Additionally, it is found that exosomal Rmrp levels are correlated with AM immune tolerance and the prognosis of patients with sepsis. These findings highlight the critical role of AEC-II-derived exosomal Rmrp in the pathogenesis of SII and secondary pneumonia. Importantly, the study suggests that exosomal Rmrp may serve as a biomarker for predicting and managing SII in clinical settings.

Indexed as

Alveolar Epithelial CellsExosomesImmune ToleranceMacrophages, AlveolarRNA, Long NoncodingSepsisAnimalsGlycolysisHumansMaleMiceMice, Inbred C57BLPhosphofructokinase-2Phosphofructokinase-2RNA, Long Noncodingalveolar macrophagesexosomal Rmrpglycolysissecondary pneumoniasepsis‐induced immunosuppression

Identifiers

PMID41178622
PMCPMC12766999

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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.