Evidence map›Paper›PMID 35768946›Full record

ArticleMicrobiology spectrum2022

Yang Jiao, Shiyang Cao, Yuan Zhang, Yafang Tan, Yazhou Zhou, Tong Wang, Yang You, Hongyan Chen, Yifan Ren, Ruifu Yang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Microbiology spectrum, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

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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 at 1 institution in 1 country.

Yang Jiao *State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, China.
Shiyang Cao *State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, China.
Yuan ZhangState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, China.
Yafang TanState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, China.
Yazhou ZhouState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, China.
Tong WangState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, China.
Yang YouState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, China.
Hongyan ChenState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, China.
Yifan RenState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, China.
Ruifu YangState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, China.
Zongmin DuState Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Microbiology and Epidemiology, Beijing, China.ORCID 0000-0002-0037-1616
Institute of Microbiology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Manipulating mitochondrial homeostasis is essential for host defense against infection and pathogen survival in cells. This study reports for the first time that Y. pestis infection caused mitochondria damage that subsequently leads to the activation of Pink1/Parkin-independent mitophagy in macrophage, and the effector YopH from the type III secretion system was required for these effects. The generation of mitochondrial reactive oxygen species (mROS) by damaged mitochondria enhances the antibacterial activity of macrophages against Y. pestis and promotes apoptosis of the infected cells. Therefore, Y. pestis-induced mitophagy was employed to eliminate dysfunctional mitochondria and relieve the mROS accumulation. This study reveals a novel role for YopH of Y. pestis in damaging host macrophage mitochondria during plague infection and underlines the vital role of mitophagy in maintaining mitochondrial homeostasis by clearing bacteria-damaged mitochondria. The results show that mitophagy or mitochondrial fission manipulation could be used as a new strategy to treat plague.

Indexed as

PlagueYersinia pestisAnti-Bacterial AgentsHomeostasisHumansMitochondriaMitophagyUbiquitin-Protein LigasesAnti-Bacterial AgentsUbiquitin-Protein Ligasesmitochondrial dysfunctionmitophagymROSplagueYersinia pestisYopH

Identifiers

PMID35768946
PMCPMC9241946
OpenAlexW4281728027

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.