CAPN1 Promotes Pseudomonas aeruginosa-Induced Infection by Interacting with TFEB and Inhibiting Autophagy.

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

3 citing papers in PubMed.

Infection and immunity · 2026
Article
Extracellular Mitochondrial Components as Emerging Biomarkers and Therapeutic Targets in Human Diseases.International journal of biological sciences · 2026
Review
HLF transactivatesScience advances · 2025
Article

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

8 authors.

Yueming WuDepartment of Critical Care Medicine, The Six Affiliated Hospital of Wenzhou Medical University, Lishui, China.

Miaomiao ChenDepartment of Critical Care Medicine, The Six Affiliated Hospital of Wenzhou Medical University, Lishui, China.

Hua ChenDepartment of Critical Care Medicine, The Six Affiliated Hospital of Wenzhou Medical University, Lishui, China.

Liuhua PanDepartment of Critical Care Medicine, The Six Affiliated Hospital of Wenzhou Medical University, Lishui, China.

Jing ZhaoDepartment of Critical Care Medicine, The Six Affiliated Hospital of Wenzhou Medical University, Lishui, China.

Shunnan SunDepartment of Critical Care Medicine, The Six Affiliated Hospital of Wenzhou Medical University, Lishui, China.

Ning ZhangDepartment of Emergency Medicine, The Six Affiliated Hospital of Wenzhou Medical University, Lishui, China.

Junlong XuDepartment of Critical Care Medicine, The Six Affiliated Hospital of Wenzhou Medical University, Lishui, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAutophagy-lysosome pathways play a crucial role in the intracellular killing of pathogenic microorganisms. This study aimed to explore the mechanism by which acute lung injury (ALI) of Pseudomonas aeruginosa affects the autophagy-lysosome pathway.

methodsALI mouse models were induced by lipopolysaccharide and P. aeruginosa strain K (PAK). Lung tissue sections were stained with hematoxylin-eosin for observation. Flow cytometry was used to analyze bacteria and inflammatory cell infiltration. ELISA was performed to measure inflammatory factor levels. Transmission electron microscopy evaluated autolysosome quantity. Western blot detected levels of related proteins. Immunofluorescence evaluated LC3 expression, and the localization of TFEB in cells was observed. Co-immunoprecipitation and pull-down experiments confirmed the interaction between CAPN1 and TFEB. qRT-PCR measured capn1 and tfeb expression.

resultsMouse experiments revealed that PAK infection led to the suppression of autolysosomes in mouse lung tissue, along with increased CAPN1 expression and decreased TFEB in the lung tissue of PAK-induced pneumonia mice. CAPN1-deficient mice could reverse the impact of PAK infection on autolysosomes in mouse lung tissue. These findings were further verified by cell experiments. At a mechanistic level, CAPN1 can interact with TFEB after PAK infection and prevent its entry into the nucleus, thereby inhibiting the autophagolysosomal pathway.

conclusionCAPN1 promotes PAK-induced ALI by inhibiting the autophagy-lysosome pathway by targeting TFEB.

introductionAutophagy-lysosome pathways play a crucial role in the intracellular killing of pathogenic microorganisms. This study aimed to explore the mechanism by which acute lung injury (ALI) of Pseudomonas aeruginosa affects the autophagy-lysosome pathway.

methodsALI mouse models were induced by lipopolysaccharide and P. aeruginosa strain K (PAK). Lung tissue sections were stained with hematoxylin-eosin for observation. Flow cytometry was used to analyze bacteria and inflammatory cell infiltration. ELISA was performed to measure inflammatory factor levels. Transmission electron microscopy evaluated autolysosome quantity. Western blot detected levels of related proteins. Immunofluorescence evaluated LC3 expression, and the localization of TFEB in cells was observed. Co-immunoprecipitation and pull-down experiments confirmed the interaction between CAPN1 and TFEB. qRT-PCR measured capn1 and tfeb expression.

resultsMouse experiments revealed that PAK infection led to the suppression of autolysosomes in mouse lung tissue, along with increased CAPN1 expression and decreased TFEB in the lung tissue of PAK-induced pneumonia mice. CAPN1-deficient mice could reverse the impact of PAK infection on autolysosomes in mouse lung tissue. These findings were further verified by cell experiments. At a mechanistic level, CAPN1 can interact with TFEB after PAK infection and prevent its entry into the nucleus, thereby inhibiting the autophagolysosomal pathway.

conclusionCAPN1 promotes PAK-induced ALI by inhibiting the autophagy-lysosome pathway by targeting TFEB.

Indexed as

Acute Lung InjuryBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCalpainLungPseudomonas aeruginosaPseudomonas InfectionsAnimalsAutophagyDisease Models, AnimalHumansLipopolysaccharidesLysosomesMaleMiceMice, Inbred C57BLMice, KnockoutBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCalpainCapn1 protein, mouseLipopolysaccharidesTcfeb protein, mouseAcute lung injuryAutophagy-lysosome pathwayCAPN1TFEB