Evidence map›Paper›PMID 35153624›Full record

ReviewMediators of inflammation2022

Dysregulated Bradykinin: Mystery in the Pathogenesis of COVID-19.

Aisha Tabassum, Mohammad Shahid Iqbal, Sadia Sultan, Raghad Ali Alhuthali, Deena Ismail Alshubaili, Raghad Salah Sayyam, Lama Mohammed Abyad, Ahmed H Qasem, Ahmad F Arbaeen

Open access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
6.3field-weighted citation impact, top 3% 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

26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 41 citations in OpenAlex.

  1. Pooled it
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  4. Three-Day Icatibant on Top of Standard Care in Patients With Coronavirus Disease 2019 Pneumonia: A Randomized, Open-Label, Phase 2, Proof-of-Concept Trial.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2023
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  10. Inhibition of kinin B1 receptor alleviates SARS-CoV-2-induced long-lasting cardiovascular complications.American journal of physiology. Heart and circulatory physiology · 2025
    Article
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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

9 authors at 2 institutions in 1 country.

Aisha TabassumAssistant Professor of Pathology, Department of Laboratory Medicine, College of Applied Medical Sciences, Umm Al Qura University, Makkah, Saudi Arabia.ORCID https://orcid.org/0000-0002-2229-2345
Mohammad Shahid IqbalAssistant Professor of Pathology, Department of Laboratory Medicine, College of Applied Medical Sciences, Umm Al Qura University, Makkah, Saudi Arabia.ORCID https://orcid.org/0000-0001-6683-409X
Sadia SultanClinical Sciences Department, Fakeeh College of Medical Sciences, Jeddah, Saudi Arabia.
Raghad Ali AlhuthaliCollege of Applied Medical Sciences, Umm Al-Qura University, Makkah, Saudi Arabia.
Deena Ismail AlshubailiCollege of Applied Medical Sciences, Umm Al-Qura University, Makkah, Saudi Arabia.
Raghad Salah SayyamCollege of Applied Medical Sciences, Umm Al-Qura University, Makkah, Saudi Arabia.
Lama Mohammed AbyadCollege of Applied Medical Sciences, Umm Al-Qura University, Makkah, Saudi Arabia.
Ahmed H QasemLaboratory Medicine Department, Faculty of Applied Medical Sciences, Umm Al-Qura University, Makkah, Saudi Arabia.ORCID https://orcid.org/0000-0002-6681-5363
Ahmad F ArbaeenFaculty of Applied Medical Sciences, Department of Laboratory Medicine, Umm Al-Qura University, Makkah, Saudi Arabia.ORCID https://orcid.org/0000-0002-9736-3005
Umm al-Qura University · SASoliman Fakeeh Hospital · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The COVID-19 pandemic is rapidly spreading, and health care systems are being overwhelmed with the huge number of cases, with a good number of cases requiring intensive care. It has become imperative to develop safe and effective treatment strategies to improve survival. In this regard, understanding the pathogenesis of COVID-19 is highly important. Many hypotheses have been proposed, including the ACE/angiotensin-II/angiotensin receptor 1 pathway, the complement pathway, and the angiotensin-converting enzyme 2/mitochondrial assembly receptor (ACE2/MasR) pathway. SARS-CoV-2 binds to the ACE2 on the cell surface, downregulating the ACE2, and thus impairs the inactivation of bradykinin and des-Arg9-bradykinin. Bradykinin, a linear nonapeptide, is extensively distributed in plasma and different tissues. Kininogens in plasma and tissue are the main sources of the two vasoactive peptides called bradykinin and kallidin. However, the role of the dysregulated bradykinin pathway is less explored in the pathogenesis of COVID-19. Understanding the pathogenesis of COVID-19 is crucial for the development of new effective treatment approaches which interfere with these pathways. In this review, we have tried to explore the interaction between SARS-CoV-2, ACE2, bradykinin, and its metabolite des-Arg9-bradykinin in the pathogenesis of COVID-19.

Indexed as

SARS-CoV-2Angiotensin-Converting Enzyme 2BradykininCOVID-19COVID-19 Drug TreatmentHumansKallikrein-Kinin SystemReceptors, BradykininAngiotensin-Converting Enzyme 2BradykininReceptors, Bradykinin

Identifiers

PMID35153624
PMCPMC8826266
OpenAlexW4210931139

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.