Evidence map›Paper›PMID 33582450›Full record

ReviewBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2021

Induced dysregulation of ACE2 by SARS-CoV-2 plays a key role in COVID-19 severity.

Maryam Eskandari Mehrabadi, Roohullah Hemmati, Amin Tashakor, Ahmad Homaei, Masoumeh Yousefzadeh, Karim Hemati, Saman Hosseinkhani

Abstract readReview
In one paragraph

Review in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 3 pooled it
–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

50 citing papers in PubMed, 3 syntheses or guidelines pooled it.

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  17. Implications of Dysnatremia and Endocrine Disturbances in COVID-19 Patients.International journal of molecular sciences · 2024
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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

7 authors.

Maryam Eskandari MehrabadiDepartment of Biology, Faculty of Basic Sciences, Shahrekord University, Sharekord, Iran.
Roohullah HemmatiDepartment of Biology, Faculty of Basic Sciences, Shahrekord University, Sharekord, Iran; Biotechnology Research Institute, Shahrekord University, Shahrekord, Iran; COVID-19 research group, Faculty of Basic Sciences, Shahrekord Univesity, Shahrekord, Iran. Electronic address: Roohullah.hemmati@sku.ac.ir.
Amin TashakorIrish Centre for Vascular Biology, Royal College of Surgeons in Ireland, Dublin, Ireland; School of Pharmacy and Biomolecular Sciences, Royal College of Surgeons in Ireland, Dublin, Ireland.
Ahmad HomaeiDepartment of Marine Biology, Faculty of Marine Science and Technology, University of Hormozgan, Bandar Abbas, Iran.
Masoumeh YousefzadehDepartment of Biology, Payame Noor University Of Najafabad, Isfahan, Iran.
Karim HematiDepartment of Anesthesiology and Pain, Iran University of Medical Sciences, Tehran, Iran.
Saman HosseinkhaniDepartment of Biochemistry, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the cause of COVID-19, is reported to increase the rate of mortality worldwide. COVID-19 is associated with acute respiratory symptoms as well as blood coagulation in the vessels (thrombosis), heart attack and stroke. Given the requirement of angiotensin converting enzyme 2 (ACE2) receptor for SARS-CoV-2 entry into host cells, here we discuss how the downregulation of ACE2 in the COVID-19 patients and virus-induced shift in ACE2 catalytic equilibrium, change the concentrations of substrates such as angiotensin II, apelin-13, dynorphin-13, and products such as angiotensin (1-7), angiotensin (1-9), apelin-12, dynorphin-12 in the human body. Substrates accumulation ultimately induces inflammation, angiogenesis, thrombosis, neuronal and tissue damage while diminished products lead to the loss of the anti-inflammatory, anti-thrombotic and anti-angiogenic responses. In this review, we focus on the viral-induced imbalance between ACE2 substrates and products which exacerbates the severity of COVID-19. Considering the roadmap, we propose multiple therapeutic strategies aiming to rebalance the products of ACE2 and to ameliorate the symptoms of the disease.

Indexed as

COVID-19Paracrine CommunicationSARS-CoV-2Angiotensin-Converting Enzyme 2Drug DiscoveryHumansSeverity of Illness IndexAngiotensin-Converting Enzyme 2ACE2Acute Respiratory SyndromeAngiotensinCardiovascular DiseaseCOVID-19

Identifiers

PMID33582450
PMCPMC7862910

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.