Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
3.7
4.7
Journals
Biomedicines
Special Issues
Angiotensin-Converting Enzyme in Health and Diseases
share announcement

Angiotensin-Converting Enzyme in Health and Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 1055

Special Issue Editor

Dr. Sergei M. Danilov

E-Mail Website
Guest Editor
Department of Medicine, University of Illinois at Chicago, Chicago, IL, USA
Interests: angiotensin-converting enzyme; monoclonal antibodies; lung targeting; endothelial cells

Special Issue Information

Dear Colleagues,

Angiotensin I-converting enzyme (ACE, CD143) is a Zn2+ carboxydipeptidase that plays crucial roles in blood pressure regulation and the development of vascular pathology. ACE is constitutively expressed on the surface of endothelial cells, absorptive epithelial cells, neuroepithelial cells, and cells of the immune system (e.g., macrophages, dendritic cells). Numerous studies have identified ACE as a potent pro-inflammatory modulator that contributes to the recruitment of inflammatory cells into tissues by regulating chemokines and adhesion molecules. Furthermore, ACE not only functions as a cell membrane ectopeptidase but can also be secreted into the extracellular environment by activated myelomonocytic or other lineage cells, acting as a local and systemic regulator of peptides. Given its broad substrate specificity and wide tissue distribution, ACE impacts various biological processes. The well-established association of ACE with immunoinflammatory diseases presents an excellent opportunity for authors and investigators to contribute their original research or review articles to this Special Issue, entitled “Angiotensin-Converting Enzyme in Health and Diseases”. We cordially invite you to share your expertise in ACE function research in this exceptional forum.

Dr. Sergei M. Danilov
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • angiotensin I-converting enzyme (ACE)
  • blood pressure regulation
  • vascular pathology
  • endothelial cells
  • immune system cells
  • macrophages
  • dendritic cells
  • pro-inflammatory modulator
  • inflammatory cell recruitment
  • chemokines
  • adhesion molecules
  • extracellular environment

Published Papers (1 paper)

Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

20 pages, 4151 KiB  
Article
Carriers of Heterozygous Loss-of-Function ACE Mutations Are at Risk for Alzheimer’s Disease
by Sergei M. Danilov, Ivan A. Adzhubei, Alexander J. Kozuch, Pavel A. Petukhov, Isolda A. Popova, Ananyo Choudhury, Dhriti Sengupta and Steven M. Dudek
Biomedicines 2024, 12(1), 162; https://doi.org/10.3390/biomedicines12010162 - 12 Jan 2024
Viewed by 909
Abstract
We hypothesized that subjects with heterozygous loss-of-function (LoF) ACE mutations are at risk for Alzheimer’s disease because amyloid Aβ42, a primary component of the protein aggregates that accumulate in the brains of AD patients, is cleaved by ACE (angiotensin I-converting enzyme). Thus, decreased [...] Read more.
We hypothesized that subjects with heterozygous loss-of-function (LoF) ACE mutations are at risk for Alzheimer’s disease because amyloid Aβ42, a primary component of the protein aggregates that accumulate in the brains of AD patients, is cleaved by ACE (angiotensin I-converting enzyme). Thus, decreased ACE activity in the brain, either due to genetic mutation or the effects of ACE inhibitors, could be a risk factor for AD. To explore this hypothesis in the current study, existing SNP databases were analyzed for LoF ACE mutations using four predicting tools, including PolyPhen-2, and compared with the topology of known ACE mutations already associated with AD. The combined frequency of >400 of these LoF-damaging ACE mutations in the general population is quite significant—up to 5%—comparable to the frequency of AD in the population > 70 y.o., which indicates that the contribution of low ACE in the development of AD could be under appreciated. Our analysis suggests several mechanisms by which ACE mutations may be associated with Alzheimer’s disease. Systematic analysis of blood ACE levels in patients with all ACE mutations is likely to have clinical significance because available sequencing data will help detect persons with increased risk of late-onset Alzheimer’s disease. Patients with transport-deficient ACE mutations (about 20% of damaging ACE mutations) may benefit from preventive or therapeutic treatment with a combination of chemical and pharmacological (e.g., centrally acting ACE inhibitors) chaperones and proteosome inhibitors to restore impaired surface ACE expression, as was shown previously by our group for another transport-deficient ACE mutation-Q1069R. Full article
(This article belongs to the Special Issue Angiotensin-Converting Enzyme in Health and Diseases)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-1
Back to TopTop