Evidence map›Paper›PMID 37608279›Full record

ReviewJournal of biomedical science2023

ACE2 in chronic disease and COVID-19: gene regulation and post-translational modification.

Chia-Wen Wang, Huai-Chia Chuang, Tse-Hua Tan

Open access · diamondAbstract readReview
In one paragraph

Review in Journal of biomedical science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
6.4field-weighted citation impact, top 2% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. ACE2: Friend or Foe in Post-COVID-19 Neurodegeneration?International journal of molecular sciences · 2025
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Observational
  17. Article
  18. Article
  19. Review
  20. Radiotracers for Molecular Imaging of Angiotensin-Converting Enzyme 2.International journal of molecular sciences · 2024
    Review
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

3 authors at 1 institution in 1 country.

Chia-Wen Wang *Immunology Research Center, National Health Research Institutes, 35 Keyan Road, Zhunan, 35053, Taiwan.
Huai-Chia Chuang *Immunology Research Center, National Health Research Institutes, 35 Keyan Road, Zhunan, 35053, Taiwan.
Tse-Hua TanImmunology Research Center, National Health Research Institutes, 35 Keyan Road, Zhunan, 35053, Taiwan. ttan@nhri.edu.tw.ORCID http://orcid.org/0000-0003-4969-3170
National Health Research Institutes · TW

Funding

National Health Research Institutes IM-112-SP-01National Science and Technology Council NSTC-111-2320-B-400-003
6 · The paper itself

Abstract

Angiotensin-converting enzyme 2 (ACE2), a counter regulator of the renin-angiotensin system, provides protection against several chronic diseases. Besides chronic diseases, ACE2 is the host receptor for SARS-CoV or SARS-CoV-2 virus, mediating the first step of virus infection. ACE2 levels are regulated by transcriptional, post-transcriptional, and post-translational regulation or modification. ACE2 transcription is enhanced by transcription factors including Ikaros, HNFs, GATA6, STAT3 or SIRT1, whereas ACE2 transcription is reduced by the transcription factor Brg1-FoxM1 complex or ERRα. ACE2 levels are also regulated by histone modification or miRNA-induced destabilization. The protein kinase AMPK, CK1α, or MAP4K3 phosphorylates ACE2 protein and induces ACE2 protein levels by decreasing its ubiquitination. The ubiquitination of ACE2 is induced by the E3 ubiquitin ligase MDM2 or UBR4 and decreased by the deubiquitinase UCHL1 or USP50. ACE2 protein levels are also increased by the E3 ligase PIAS4-mediated SUMOylation or the methyltransferase PRMT5-mediated ACE2 methylation, whereas ACE2 protein levels are decreased by AP2-mediated lysosomal degradation. ACE2 is downregulated in several human chronic diseases like diabetes, hypertension, or lung injury. In contrast, SARS-CoV-2 upregulates ACE2 levels, enhancing host cell susceptibility to virus infection. Moreover, soluble ACE2 protein and exosomal ACE2 protein facilitate SARS-CoV-2 infection into host cells. In this review, we summarize the gene regulation and post-translational modification of ACE2 in chronic disease and COVID-19. Understanding the regulation and modification of ACE2 may help to develop prevention or treatment strategies for ACE2-mediated diseases.

Indexed as

Angiotensin-Converting Enzyme 2COVID-19Chronic DiseaseHumansProtein-Arginine N-MethyltransferasesProtein Processing, Post-TranslationalProtein Serine-Threonine KinasesSARS-CoV-2ACE2 protein, humanAngiotensin-Converting Enzyme 2MAP4K3 protein, humanPRMT5 protein, humanProtein-Arginine N-MethyltransferasesProtein Serine-Threonine KinasesACE2Angiotensin IIChronic diseaseCOVID-19GlycosylationPhosphorylationSARS-CoV-2TranscriptionUbiquitination

Identifiers

PMID37608279
PMCPMC10464117
OpenAlexW4386083985

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.