Targeting Monocytes/Macrophages to Treat Atherosclerotic Inflammation (Record no. 41589)
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| 000 -LEADER | |
|---|---|
| fixed length control field | 05013naaaa2200409uu 4500 |
| 001 - CONTROL NUMBER | |
| control field | https://directory.doabooks.org/handle/20.500.12854/73741 |
| 005 - DATE AND TIME OF LATEST TRANSACTION | |
| control field | 20220219202403.0 |
| 020 ## - INTERNATIONAL STANDARD BOOK NUMBER | |
| International Standard Book Number | 978-2-88963-599-3 |
| 020 ## - INTERNATIONAL STANDARD BOOK NUMBER | |
| International Standard Book Number | 9782889635993 |
| 024 7# - OTHER STANDARD IDENTIFIER | |
| Standard number or code | 10.3389/978-2-88963-599-3 |
| Terms of availability | doi |
| 041 0# - LANGUAGE CODE | |
| Language code of text/sound track or separate title | English |
| 042 ## - AUTHENTICATION CODE | |
| Authentication code | dc |
| 072 #7 - SUBJECT CATEGORY CODE | |
| Subject category code | PD |
| Source | bicssc |
| 072 #7 - SUBJECT CATEGORY CODE | |
| Subject category code | MMG |
| Source | bicssc |
| 100 1# - MAIN ENTRY--PERSONAL NAME | |
| Personal name | Corti, Alessandro |
| Relationship | edt |
| 245 10 - TITLE STATEMENT | |
| Title | Targeting Monocytes/Macrophages to Treat Atherosclerotic Inflammation |
| 260 ## - PUBLICATION, DISTRIBUTION, ETC. | |
| Name of publisher, distributor, etc. | Frontiers Media SA |
| Date of publication, distribution, etc. | 2020 |
| 300 ## - PHYSICAL DESCRIPTION | |
| Extent | 1 electronic resource (127 p.) |
| 506 0# - RESTRICTIONS ON ACCESS NOTE | |
| Terms governing access | Open Access |
| Source of term | star |
| Standardized terminology for access restriction | Unrestricted online access |
| 520 ## - SUMMARY, ETC. | |
| Summary, etc. | It is by now widely recognized that atherosclerosis – with its burden of consequences in cerebro- and cardiovascular diseases – is just a chronic inflammatory process of the arterial wall. A very peculiar, complex and as yet still poorly understood process, upon which hundreds of scientists from several different fields are continuously concentrating their investigative efforts in search of possible leads to therapeutic approaches. Initiation of the disease is given by deposition of lipid in the intimal layers, resulting in endothelial activation and infiltration of blood-derived mononuclear cells. These mature into macrophages, become activated, express scavenger receptors such as SR-A and CD36 and ingest the oxidized lipoprotein accumulating in the lesion. Macrophages thus represent an obvious target for intervention, as they play a crucial role in the progression of the atherosclerotic inflammation. Studies have shown that hypercholesterolaemia can increase monocyte mobilisation from bone marrow into the circulation, and several chemokines and their receptors are involved in the recruitment of blood borne monocytes into the arterial wall. Monocyte-derived macrophages are capable of sustaining their local proliferation, but resident macrophages possibly also participate in progression of the disease. Remarkably, smooth muscle cells can acquire macrophage-like features during atherogenesis, including the ability to uptake lipid, thus becoming a significant proportion of the CD68+ so called ‘foam cells’. Lipid-laden macrophages induce extracellular matrix degradation, while lipid uptake eventually causes their death with formation of a necrotic core. The efficiency in clearance of dead cells by phagocytes (efferocytosis), can also be considered as a determinant of plaque vulnerability. An important feature of macrophages is their great plasticity and functional diversity in response to signals from the plaque microenvironment. Several such ‘signals’ (cholesterol, oxidative stress, hypoxia, cytokines…) can in fact modulate cell differentiation at transcriptional and epigenetic levels, thus altering the balance between the effector vs. reparative functions of macrophages. A whole gamut of specific subsets are thus originated, which appear to be simultaneously present in lesions with proportions that vary according to their location, the disease stage, and the presence of additional cell types such as e.g. dendritic cells. The result is a multiplicity of potential pharmacological targets, representing a major obstacle for the devisement of therapeutic strategies. Experimental approaches have been attempted in diverse directions: e.g. modulating the macrophage phenotype to an anti-inflammatory and resolving state, or blocking pro-inflammatory cytokines that macrophages produce, or alternatively enhancing efferocytosis in order to favour the resolution of inflammation and stabilization of plaques. Blocking monocyte recruitment was proposed in order to hinder the initial steps of atherogenesis. Other treatments were aimed to inhibiting local proliferation of pro-inflammatory macrophages. Specific targeting of macrophages has however to date not yet provided significant, translational results. The present Research Topic collects articles to help unravel the complexity of macrophage behaviour in atherosclerosis and identify innovative pharmacological approaches. |
| 540 ## - TERMS GOVERNING USE AND REPRODUCTION NOTE | |
| Terms governing use and reproduction | Creative Commons |
| Use and reproduction rights | https://creativecommons.org/licenses/by/4.0/ |
| Source of term | cc |
| -- | https://creativecommons.org/licenses/by/4.0/ |
| 546 ## - LANGUAGE NOTE | |
| Language note | English |
| 650 #7 - SUBJECT ADDED ENTRY--TOPICAL TERM | |
| Topical term or geographic name entry element | Science: general issues |
| Source of heading or term | bicssc |
| 650 #7 - SUBJECT ADDED ENTRY--TOPICAL TERM | |
| Topical term or geographic name entry element | Pharmacology |
| Source of heading or term | bicssc |
| 653 ## - INDEX TERM--UNCONTROLLED | |
| Uncontrolled term | monocytes/macrophages |
| 653 ## - INDEX TERM--UNCONTROLLED | |
| Uncontrolled term | inflammation |
| 653 ## - INDEX TERM--UNCONTROLLED | |
| Uncontrolled term | foam cell formation |
| 653 ## - INDEX TERM--UNCONTROLLED | |
| Uncontrolled term | smooth muscle cells |
| 653 ## - INDEX TERM--UNCONTROLLED | |
| Uncontrolled term | atherosclerosis progression |
| 700 1# - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Gaucher, Caroline |
| Relationship | edt |
| 700 1# - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Pompella, Alfonso |
| Relationship | edt |
| 700 1# - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Corti, Alessandro |
| Relationship | oth |
| 700 1# - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Gaucher, Caroline |
| Relationship | oth |
| 700 1# - ADDED ENTRY--PERSONAL NAME | |
| Personal name | Pompella, Alfonso |
| Relationship | oth |
| 856 40 - ELECTRONIC LOCATION AND ACCESS | |
| Host name | www.oapen.org |
| Uniform Resource Identifier | <a href="https://www.frontiersin.org/research-topics/8456/targeting-monocytesmacrophages-to-treat-atherosclerotic-inflammation">https://www.frontiersin.org/research-topics/8456/targeting-monocytesmacrophages-to-treat-atherosclerotic-inflammation</a> |
| Access status | 0 |
| Public note | DOAB: download the publication |
| 856 40 - ELECTRONIC LOCATION AND ACCESS | |
| Host name | www.oapen.org |
| Uniform Resource Identifier | <a href="https://directory.doabooks.org/handle/20.500.12854/73741">https://directory.doabooks.org/handle/20.500.12854/73741</a> |
| Access status | 0 |
| Public note | DOAB: description of the publication |
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