Evidence map›Paper›PMID 33404363›Full record

ReviewAmerican journal of physiology. Lung cellular and molecular physiology2021

Kinins and chymase: the forgotten components of the renin-angiotensin system and their implications in COVID-19 disease.

Zaid Abassi, Karl Skorecki, Dalit B Hamo-Giladi, Etty Kruzel-Davila, Samuel N Heyman

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Lung cellular and molecular physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 31 citations in OpenAlex.

  1. Mast cell mediators in hereditary angioedema.Orphanet journal of rare diseases · 2026
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  12. COVID-lateral damage: cardiovascular manifestations of SARS-CoV-2 infection.Translational research : the journal of laboratory and clinical medicine · 2022
    Review
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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

5 authors at 3 institutions in 1 country.

Zaid AbassiDepartment of Physiology and Biophysics, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Karl SkoreckiThe Azrieli Faculty of Medicine, Bar-Ilan University, Safed, Israel.
Dalit B Hamo-GiladiDepartment of Physiology and Biophysics, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Etty Kruzel-DavilaDepartment of Nephrology, Rambam Health Care Campus, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.ORCID 0000-0002-7208-5707
Samuel N HeymanDepartment of Medicine, Hadassah Hebrew University Hospital, Jerusalem, Israel.
Technion – Israel Institute of Technology · ILBar-Ilan University · ILHebrew University of Jerusalem · IL

Funding

Israeli Science Foundation 182115Israeli Science Foundation 544/18The Kaylie Family Foundation
6 · The paper itself

Abstract

The unique clinical features of COVID-19 disease present a formidable challenge in the understanding of its pathogenesis. Within a very short time, our knowledge regarding basic physiological pathways that participate in SARS-CoV-2 invasion and subsequent organ damage have been dramatically expanded. In particular, we now better understand the complexity of the renin-angiotensin-aldosterone system (RAAS) and the important role of angiotensin converting enzyme (ACE)-2 in viral binding. Furthermore, the critical role of its major product, angiotensin (Ang)-(1-7), in maintaining microcirculatory balance and in the control of activated proinflammatory and procoagulant pathways, generated in this disease, have been largely clarified. The kallikrein-bradykinin (BK) system and chymase are intensively interwoven with RAAS through many pathways with complex reciprocal interactions. Yet, so far, very little attention has been paid to a possible role of these physiological pathways in the pathogenesis of COVID-19 disease, even though BK and chymase exert many physiological changes characteristic to this disorder. Herein, we outline the current knowledge regarding the reciprocal interactions of RAAS, BK, and chymase that are probably turned-on in COVID-19 disease and participate in its clinical features. Interventions affecting these systems, such as the inhibition of chymase or blocking BKB1R/BKB2R, might be explored as potential novel therapeutic strategies in this devastating disorder.

Indexed as

Renin-Angiotensin SystemChymasesCOVID-19HumansKininsSARS-CoV-2ChymasesKininsACE2bradykininchymaseCOVID-19SARS-CoV-2

Identifiers

PMID33404363
PMCPMC7938643
OpenAlexW3119445497

What Socratic 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 Socratic graph.