Evidence map›Paper›PMID 35466734›Full record

ArticleExperimental biology and medicine (Maywood, N.J.)2022

Lipocalin-2, S100A8/A9, and cystatin C: Potential predictive biomarkers of cardiovascular complications in COVID-19.

Anamika Gupta, Abaher O Al-Tamimi, Rabih Halwani, Hend Alsaidi, Meganathan Kannan, Firdos Ahmad

Open access · bronzeAbstract read
In one paragraph

Article in Experimental biology and medicine (Maywood, N.J.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
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  12. Circulating H-FABP as a biomarker of frailty in patients with chronic heart failure.Experimental biology and medicine (Maywood, N.J.) · 2023
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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 3 institutions in 2 countries.

Anamika GuptaCardiovascular Research Group, Sharjah Institute for Medical Research, University of Sharjah, Sharjah 27272, UAE.
Abaher O Al-TamimiCardiovascular Research Group, Sharjah Institute for Medical Research, University of Sharjah, Sharjah 27272, UAE.
Rabih HalwaniDepartment of Clinical Sciences, College of Medicine, University of Sharjah, Sharjah 27272, UAE.
Hend AlsaidiDepartment of Internal Medicine, Rashid Hospital, Dubai 4545, UAE.
Meganathan KannanBlood and Vascular Biology Research Lab, Department of Life Sciences, Central University of Tamil Nadu, Thiruvarur 610005, India.
Firdos AhmadCardiovascular Research Group, Sharjah Institute for Medical Research, University of Sharjah, Sharjah 27272, UAE.ORCID 0000-0001-6530-6068
University of Sharjah · AECentral University of Tamil Nadu · INRashid Hospital · AE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe coronavirus (SARS-COV-2) infection often leads to systemic inflammation accompanied by cardiovascular complications including venous thromboembolism (VTE). However, it is largely undefined if inflammatory markers such as lipocalin-2 (LNC2), calprotectin (S100A8/A9), and cystatin C (CST3), previously linked with VTE, play roles in cardiovascular complications and advancement of COVID-19 severity. To investigate the same, hospitalized moderate and severe (presented pneumonia and required intensive care) COVID-19 patients were recruited. The levels of plasma LNC2, S100A8/A9, CST3, myoglobin, and cardiac Troponin I (cTnI) were assessed through enzyme-linked immunosorbent assay (ELISA). The investigation revealed a significantly upregulated level of plasma LNC2 at the moderate stage of SARS-CoV-2 infection. In contrast, the levels of S100A8/A9 and CST3 in moderate patients were comparable to healthy controls; however, a profound induction was observed only in severe COVID-19 patients. The tissue injury marker myoglobin was unchanged in moderate patients; however, a significantly elevated level was observed in the critically ill COVID-19 patients. In contrast, cTnI level was unchanged both in moderate and severe patients. Analysis revealed a positive correlation between the levels of S100A8/A9 and CST3 with myoglobin in COVID-19. In silico analysis predicted interactions of S100A8/A9 with toll-like receptor 4 (TLR-4), MyD88 LY96, and LCN2 with several other inflammatory mediators including MMP2, MMP9, TIMP1, and interleukins (IL-6, IL-17A, and IL-10). In summary, early induction of LCN2 likely plays a role in advancing the COVID-19 severity. A positive correlation of S100A8/A9 and CST3 with myoglobin suggests that these proteins may serve as predictive biomarkers for thromboembolism and tissue injury in COVID-19.

Indexed as

COVID-19Venous ThromboembolismBiomarkersCalgranulin ACalgranulin BCystatin CHumansLipocalin-2MyoglobinSARS-CoV-2BiomarkersCalgranulin ACalgranulin BCST3 protein, humanCystatin CLCN2 protein, humanLipocalin-2MyoglobinS100A8 protein, humanS100A9 protein, humancalprotectincardiovascularCOVID-19cystatin Clipocalin-2thromboembolism

Identifiers

PMID35466734
PMCPMC9379606
OpenAlexW4224864749

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.