Evidence map›Paper›PMID 41258714›Full record

ArticleMicrobiology spectrum2026

Cathepsin S contributes to influenza-induced lung injury by driving inflammation, promoting apoptosis, and disrupting epithelial barrier integrity.

Tianxin Ma, Chunguang Yang, Yang Wang, Chuanmeizi Tu, Jiawei Zhang, Kailin Mai, Shengzhen Wu, Hongxuan Zhou, Shengfeng Li, Sulan Ye and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Microbiology spectrum, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

16 authors.

Tianxin Ma *State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.ORCID 0009-0007-3549-1072
Chunguang Yang *State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Yang Wang *State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.ORCID 0000-0002-6527-864X
Chuanmeizi Tu *State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Jiawei ZhangState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Kailin MaiState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Shengzhen WuState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Hongxuan ZhouDepartment of Critical Care, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Shengfeng LiDepartment of Critical Care, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Sulan YeState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Lixi LiangState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Qingsheng HuangState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Zhenhui ZhangDepartment of Critical Care, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.ORCID 0000-0002-2801-8865
Zhengshi LinState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.ORCID 0009-0005-5964-0760
Weiqi PanState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.ORCID 0009-0003-1989-4008
Zifeng YangState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.ORCID 0000-0002-2681-4171

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Influenza virus infection causes significant morbidity and mortality worldwide, with severe cases often driven by excessive host inflammatory responses and disruption of epithelial barrier function. Here, we identified cathepsin S (CTSS), a lysosomal cysteine protease, as a key mediator of influenza-induced lung injury. Influenza virus infection upregulated CTSS in a time-dependent and dose-dependent manner, leading to lysosomal membrane permeabilization and cytoplasmic release of CTSS, which correlated with increased apoptosis and loss of epithelial barrier integrity. Knockdown of CTSS reduced proinflammatory cytokine production, apoptosis, and barrier disruption in A549 cells. Air-liquid interface airway epithelial cultures further validated the essential role of CTSS in preserving epithelial barrier integrity.

Indexed as

ApoptosisCathepsinsInfluenza, HumanLung InjuryOrthomyxoviridae InfectionsA549 CellsAnimalsCytokinesDisease Models, AnimalEpithelial CellsHumansInflammationLungMiceMice, Inbred C57BLTumor Necrosis Factor-alphacathepsin SCathepsinsCytokinesTumor Necrosis Factor-alphaapoptosiscathepsin Sepithelial barrierinflammatory response

Identifiers

PMID41258714
PMCPMC12772400

What OpenQuestion holds

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LicenceCC BY
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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 OpenQuestion graph.