Evidence map›Paper›PMID 35067165›Full record

ArticleAutophagy2022

SARS-CoV-2 targets the lysosome to mediate airway inflammatory cell death.

Xiao Sun, Jun Yu, Sunny Hei Wong, Matthew Tak Vai Chan, Lin Zhang, William Ka Kei Wu

Open access · greenAbstract readComment
In one paragraph

Article in Autophagy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 13% of its field
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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Programmed cell death in human respiratory syncytial virus infection.Frontiers in cellular and infection microbiology · 2025
    Pooled it
  2. Review
  3. Differential COVID-19 Outcomes Across Lysosomal Disorders.medRxiv : the preprint server for health sciences · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 3 countries.

Xiao SunDepartment of Anaesthesia and Intensive Care and Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong Administrative Region, China.
Jun YuState Key Laboratory of Digestive Diseases, Li Ka Shing Institute of Health Sciences, the Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.
Sunny Hei WongState Key Laboratory of Digestive Diseases, Li Ka Shing Institute of Health Sciences, the Chinese University of Hong Kong, Hong Kong Special Administrative Region, China.
Matthew Tak Vai ChanDepartment of Anaesthesia and Intensive Care and Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong Administrative Region, China.
Lin ZhangDepartment of Anaesthesia and Intensive Care and Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong Administrative Region, China.
William Ka Kei WuDepartment of Anaesthesia and Intensive Care and Peter Hung Pain Research Institute, The Chinese University of Hong Kong, Hong Kong Administrative Region, China.
Chinese University of Hong Kong · CNUniversity of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As the coronavirus disease 2019 (COVID-19) pandemic continues to wreak havoc, researchers around the globe are working together to understand how the responsible agent - severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) damages the respiratory system and other organs. Macroautophagy/autophagy is an innate immune response against viral infection and is known to be manipulated by positive-strand RNA viruses, including SARS-CoV-2. Nevertheless, the link between autophagic subversion and cell death or inflammation in COVID-19 remains unclear. Emerging evidence suggests that SARS-CoV-2 could trigger pyroptosis, a form of inflammatory programmed cell death characterized by the activation of inflammasomes and CASP1 (caspase 1) and the formation of transmembrane pores by GSDMD (gasdermin D). In this connection, autophagic flux impairment is a known activator of inflammasomes. This prompted us to investigate if SARS-CoV-2 could target autophagy to induce inflammasome-dependent pyroptosis in lung epithelial cells.

Indexed as

COVID-19Vacuolar Proton-Translocating ATPasesAutophagyCaspase 1HumansInflammasomesInterleukin-1betaLungLysosomesNLR Family, Pyrin Domain-Containing 3 ProteinPyroptosisSARS-CoV-2ATP6AP1 protein, humanCaspase 1InflammasomesInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinVacuolar Proton-Translocating ATPasesCell deathCovidlungNSPpyroptosis

Identifiers

PMID35067165
PMCPMC9397439
OpenAlexW4206979590

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.