Evidence map›Paper›PMID 36246577›Full record

ArticleiScience2022

Metabolic modeling of single bronchoalveolar macrophages reveals regulators of hyperinflammation in COVID-19.

Qiuchen Zhao, Zhenyang Yu, Shengyuan Zhang, Xu-Rui Shen, Hao Yang, Yangyang Xu, Yang Liu, Lin Yang, Qing Zhang, Jiaqi Chen and 10 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 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

20 authors at 7 institutions in 2 countries.

Qiuchen ZhaoDepartment of Radiation and Medical Oncology, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan 430071, China.
Zhenyang YuDepartment of Radiation and Medical Oncology, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan 430071, China.
Shengyuan ZhangInstitute for Hepatology, National Clinical Research Center for Infectious Disease, Shenzhen Third People's Hospital, the Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, Shenzhen 518112, China.
Xu-Rui ShenCAS Key Laboratory of Special Pathogens and State Key Laboratory of Virology, Wuhan Institute of Virology, Center for Biosafety Mega-Science, Chinese Academy of Sciences, Wuhan, China.
Hao YangDepartment of Radiation and Medical Oncology, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan 430071, China.
Yangyang XuDepartment of Radiation and Medical Oncology, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan 430071, China.
Yang LiuInstitute for Hepatology, National Clinical Research Center for Infectious Disease, Shenzhen Third People's Hospital, the Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, Shenzhen 518112, China.
Lin YangDepartment of General Surgery, Xuzhou Mine Hospital, Xuzhou 221000, China.
Qing ZhangCancer Institute, Xuzhou Medical University, Xuzhou 221000, China.
Jiaqi ChenSchool of Computer Sciences, Wuhan University, Wuhan 430071, China.
Mengmeng LuDepartment of Radiation and Medical Oncology, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan 430071, China.
Fei LuoDepartment of Radiation and Medical Oncology, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan 430071, China.
Mingming HuFrontier Science Center for Immunology and Metabolism, Department of Pulmonary and Critical Care Medicine, Zhongnan Hospital of Wuhan University, State Key Laboratory of Virology, Wuhan University, Wuhan 430071, China.
Yan GongDepartment of Biological Repositories, Zhongnan Hospital of Wuhan University, Wuhan 430071, China.
Conghua XieDepartment of Radiation and Medical Oncology, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan 430071, China.
Peng ZhouCAS Key Laboratory of Special Pathogens and State Key Laboratory of Virology, Wuhan Institute of Virology, Center for Biosafety Mega-Science, Chinese Academy of Sciences, Wuhan, China.
Li WangFrontier Science Center for Immunology and Metabolism, Department of Pulmonary and Critical Care Medicine, Zhongnan Hospital of Wuhan University, State Key Laboratory of Virology, Wuhan University, Wuhan 430071, China.
Lishan SuDivision of Virology, Pathogenesis and Cancer, Institute of Human Virology and Department of Pharmacology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Zheng ZhangInstitute for Hepatology, National Clinical Research Center for Infectious Disease, Shenzhen Third People's Hospital, the Second Affiliated Hospital, School of Medicine, Southern University of Science and Technology, Shenzhen 518112, China.
Liang ChengDepartment of Radiation and Medical Oncology, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan 430071, China.
Wuhan University · CNZhongnan Hospital of Wuhan University · CNSouthern University of Science and Technology · CNXuzhou Medical College · CNChinese Academy of Sciences · CNUniversity of Maryland, Baltimore · USWuhan Institute of Virology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SARS-CoV-2 infection induces imbalanced immune response such as hyperinflammation in patients with severe COVID-19. Here, we studied the immunometabolic regulatory mechanisms for the pathogenesis of COVID-19. We depicted the metabolic landscape of immune cells, especially macrophages, from bronchoalveolar lavage fluid of patients with COVID-19 at single-cell level. We found that most metabolic processes were upregulated in macrophages from lungs of patients with mild COVID-19 compared to cells from healthy controls, whereas macrophages from severe COVID-19 showed downregulation of most of the core metabolic pathways including glutamate metabolism, fatty acid oxidation, citrate cycle, and oxidative phosphorylation, and upregulation of a few pathways such as glycolysis. Rewiring cellular metabolism by amino acid supplementation, glycolysis inhibition, or PPARγ stimulation reduces inflammation in macrophages stimulated with SARS-CoV-2. Altogether, this study demonstrates that metabolic imbalance of bronchoalveolar macrophages may contribute to hyperinflammation in patients with severe COVID-19 and provides insights into treating COVID-19 by immunometabolic modulation.

Indexed as

BioinformaticsBiological sciencesImmunologyVirology

Identifiers

PMID36246577
PMCPMC9549388
OpenAlexW4304161111

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.