Evidence map›Paper›PMID 38862942›Full record

ArticleMolecular medicine (Cambridge, Mass.)2024

Multi-omics analysis uncovered systemic lupus erythematosus and COVID-19 crosstalk.

Zekai Nian, Yicheng Mao, Zexia Xu, Ming Deng, Yixi Xu, Hanlu Xu, Ruoyao Chen, Yiliu Xu, Nan Huang, Feiyang Mao and 7 more

Abstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

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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

17 authors.

Zekai Nian *Second Clinical College, Wenzhou Medical University, Wenzhou, China.
Yicheng Mao *Ophthalmology College, Wenzhou Medical University, Wenzhou, China.
Zexia Xu *Department of Nephrology, First Affiliated Hospital, Wenzhou Medical University, Wenzhou, China.
Ming Deng *Public Health and Management College, Wenzhou Medical University, Wenzhou, China.
Yixi XuSchool of Public Administration, Hangzhou Normal University, Hangzhou, China.
Hanlu XuOphthalmology College, Wenzhou Medical University, Wenzhou, China.
Ruoyao ChenSecond Clinical College, Wenzhou Medical University, Wenzhou, China.
Yiliu XuResearch Center of Fluid Machinery Engineering and Technology, Jiangsu University, Zhenjiang, China.
Nan HuangPublic Health and Management College, Wenzhou Medical University, Wenzhou, China.
Feiyang MaoSecond Clinical College, Wenzhou Medical University, Wenzhou, China.
Chenyu XuWenzhou Collaborative Innovation Center of Gastrointestinal Cancer in Basic Research and Precision Medicine, Wenzhou Key Laboratory of Cancer-Related Pathogens and Immunity, Department of Microbiology and Immunology, Institute of Molecular Virology and Immunology, Institute of Tropical Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.
Yulin WangPublic Health and Management College, Wenzhou Medical University, Wenzhou, China.
Mengyuan NiuWenzhou Collaborative Innovation Center of Gastrointestinal Cancer in Basic Research and Precision Medicine, Wenzhou Key Laboratory of Cancer-Related Pathogens and Immunity, Department of Microbiology and Immunology, Institute of Molecular Virology and Immunology, Institute of Tropical Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China.
Aqiong ChenDepartment of Rheumatology, Ningbo Medical Center Lihuili Hospital, Ningbo, China.
Xiangyang XueWenzhou Collaborative Innovation Center of Gastrointestinal Cancer in Basic Research and Precision Medicine, Wenzhou Key Laboratory of Cancer-Related Pathogens and Immunity, Department of Microbiology and Immunology, Institute of Molecular Virology and Immunology, Institute of Tropical Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China. wzxxy001@163.com.
Huidi ZhangDepartment of Nephrology, First Affiliated Hospital, Wenzhou Medical University, Wenzhou, China. hd_zhang@163.com.
Gangqiang GuoWenzhou Collaborative Innovation Center of Gastrointestinal Cancer in Basic Research and Precision Medicine, Wenzhou Key Laboratory of Cancer-Related Pathogens and Immunity, Department of Microbiology and Immunology, Institute of Molecular Virology and Immunology, Institute of Tropical Medicine, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, China. gangqiangg@wmu.edu.cn.ORCID 0000-0001-8031-7937

Funding

National Innovation and Entrepreneurship Training Program for College Students 202210343023National Natural Science Foundation of China Grants 32200476National Natural Science Foundation of China Grants 82001705Ningbo Natural Science Foundation 2022J257Wenzhou Municipal Science and Technology Bureau Y20220044Zhejiang Provincial Natural Science Foundation of China LQ23C060002
6 · The paper itself

Abstract

backgroundStudies have highlighted a possible crosstalk between the pathogeneses of COVID-19 and systemic lupus erythematosus (SLE); however, the interactive mechanisms remain unclear. We aimed to elucidate the impact of COVID-19 on SLE using clinical information and the underlying mechanisms of both diseases.

methodsRNA-seq datasets were used to identify shared hub gene signatures between COVID-19 and SLE, while genome-wide association study datasets were used to delineate the interaction mechanisms of the key signaling pathways. Finally, single-cell RNA-seq datasets were used to determine the primary target cells expressing the shared hub genes and key signaling pathways.

resultsCOVID-19 may affect patients with SLE through hematologic involvement and exacerbated inflammatory responses. We identified 14 shared hub genes between COVID-19 and SLE that were significantly associated with interferon (IFN)-I/II. We also screened and obtained four core transcription factors related to these hub genes, confirming the regulatory role of the IFN-I/II-mediated Janus kinase/signal transducers and activators of transcription (JAK-STAT) signaling pathway on these hub genes. Further, SLE and COVID-19 can interact via IFN-I/II and IFN-I/II receptors, promoting the levels of monokines, including interleukin (IL)-6/10, tumor necrosis factor-α, and IFN-γ, and elevating the incidence rate and risk of cytokine release syndrome. Therefore, in SLE and COVID-19, both hub genes and core TFs are enriched within monocytes/macrophages.

conclusionsThe interaction between SLE and COVID-19 promotes the activation of the IFN-I/II-triggered JAK-STAT signaling pathway in monocytes/macrophages. These findings provide a new direction and rationale for diagnosing and treating patients with SLE-COVID-19 comorbidity.

Indexed as

COVID-19Genome-Wide Association StudyLupus Erythematosus, SystemicSARS-CoV-2Signal TransductionFemaleGene Expression ProfilingHumansJanus KinasesMaleMultiomicsSTAT Transcription FactorsTranscriptomeJanus KinasesSTAT Transcription FactorsCOVID-19Cytokine release syndromeInterferonJAK-STATMonokineSystemic lupus erythematosus

Identifiers

PMID38862942
PMCPMC11167821

What Socratic holds

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Registered trials

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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 Socratic graph.