Evidence map›Paper›PMID 37047115›Full record

ReviewInternational journal of molecular sciences2023

Prospective Roles of Tumor Necrosis Factor-Alpha (TNF-α) in COVID-19: Prognosis, Therapeutic and Management.

Zarina Mohd Zawawi, Jeevanathan Kalyanasundram, Rozainanee Mohd Zain, Ravindran Thayan, Dayang Fredalina Basri, Wei Boon Yap

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 2 pooled it
15.7field-weighted citation impact, top 1% 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

53 citing papers in PubMed, 2 syntheses or guidelines pooled it, 81 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

6 authors at 2 institutions in 1 country.

Zarina Mohd ZawawiVirology Unit, Infectious Disease Research Centre, Institute for Medical Research, National Institutes of Health, Ministry of Health, Bandar Setia Alam, Shah Alam 40170, Malaysia.
Jeevanathan KalyanasundramVirology Unit, Infectious Disease Research Centre, Institute for Medical Research, National Institutes of Health, Ministry of Health, Bandar Setia Alam, Shah Alam 40170, Malaysia.
Rozainanee Mohd ZainVirology Unit, Infectious Disease Research Centre, Institute for Medical Research, National Institutes of Health, Ministry of Health, Bandar Setia Alam, Shah Alam 40170, Malaysia.
Ravindran ThayanVirology Unit, Infectious Disease Research Centre, Institute for Medical Research, National Institutes of Health, Ministry of Health, Bandar Setia Alam, Shah Alam 40170, Malaysia.
Dayang Fredalina BasriCenter for Diagnostic, Therapeutic and Investigative Studies, Faculty of Health Sciences, Universiti Kebangsaan Malaysia, Jalan Raja Muda Abdul Aziz, Kuala Lumpur 50300, Malaysia.
Wei Boon YapCenter for Toxicology & Health Risk Studies, Faculty of Health Sciences, Universiti Kebangsaan Malaysia, Jalan Raja Muda Abdul Aziz, Kuala Lumpur 50300, Malaysia.ORCID 0000-0003-2449-8395
Ministry of Health · MYNational University of Malaysia · MY

Funding

Ministry of Health Malaysia NMRR ID-22-01257-WCOMinistry of Higher Education Malaysia FRGS/1/2021/STG03/UKM/02/2
6 · The paper itself

Abstract

The coronavirus disease 2019 (COVID-19) became a worldwide concern at the beginning of 2020 and has affected millions. Several previous studies revealed the impact of the imbalanced innate immune response on the progression of COVID-19 and its disease outcomes. High levels of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α) and interleukins are produced readily by innate immune cells to fight Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2) infections. Nonetheless, cytokine-mediated inflammatory events are also linked to detrimental lung injury and respiratory failure, which can result in deaths among COVID-19 patients. TNF-α is amongst the early cytokines produced to mediate proinflammatory responses and enhance immune cell infiltration in response to SARS-CoV-2 infections. In COVID-19, TNF-α-mediated inflammation can cause detrimental tissue damage and gradually promotes lung fibrosis, which later results in pneumonia, pulmonary edema, and acute respiratory distress syndrome. This review, therefore, aims to deliberate the immunomodulatory roles of TNF-α in promoting inflammation and its relation with COVID-19 morbidity and mortality. In addition, this review also proposes the potential of TNF-α as a biomarker for the prognosis of severe COVID-19 and its related complications and as a molecular target for anti-TNF-α therapy.

Indexed as

COVID-19CytokinesHumansInflammationSARS-CoV-2Tumor Necrosis Factor-alphaTumor Necrosis Factor InhibitorsCytokinesTumor Necrosis Factor-alphaTumor Necrosis Factor InhibitorsCOVID-19cytokinesinflammationSARS-CoV-2TNF-α

Identifiers

PMID37047115
PMCPMC10094668
OpenAlexW4360860138

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.