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Cells
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Phagocytosis of Apoptotic Cells as Central Driver of the Resolution...
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Phagocytosis of Apoptotic Cells as Central Driver of the Resolution of Inflammation and the Restoration of Tissue Integrity

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (20 May 2022) | Viewed by 13624

Special Issue Editor

Prof. Zsuzsa Szondy

E-Mail Website
Guest Editor
Department of Dental Biochemistry, Faculty of Dentistry, University of Debrecen, H-4012 Debrecen, Hungary
Interests: apoptosis signaling

Special Issue Information

Dear Colleagues,

Inflammation is a biological response of the mammalian body to pathogen entry and to necrotic cell death. Following pathogen or dead cell removal, efficient resolution is important not only for the termination of the inflammatory response but also for the restoration of tissue integrity. Unresolved chronic inflammation in the long term leads to irreversible tissue damage. A central process leading to the resolution of inflammation is the phagocytosis of dying cells by macrophages, known as efferocytosis. Efferocytosis is not only a waste disposal mechanism (uptake and degradation of the apoptotic cells), but it also induces the conversion of pro-inflammatory macrophages to pro-resolving macrophages which drive the termination of inflammation as well as tissue repair. Increasing evidence indicates that the impaired clearance of apoptotic cells might contribute at some point to the development of all chronic inflammatory diseases, including obesity and autoimmunity. In this Special Issue we aim to collect a series of original studies and review papers to highlight mechanisms through which this macrophage phenotype conversion takes place and orchestrates the resolution of inflammation and tissue repair.

Prof. Zsuzsa Szondy
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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • efferocytosis
  • chronic inflammatory disease
  • phagocytic receptors
  • nuclear receptors
  • anti-inflammatory cytokines
  • growth factors
  • resolvins
  • autoimmune diseases
  • resolution of inflammation

Published Papers (3 papers)

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Research

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15 pages, 2029 KiB  
Article
Regenerating Skeletal Muscle Compensates for the Impaired Macrophage Functions Leading to Normal Muscle Repair in Retinol Saturase Null Mice
by Nastaran Tarban, Hajnalka Halász, Péter Gogolák, Éva Garabuczi, Alexander R. Moise, Krzysztof Palczewski, Zsolt Sarang and Zsuzsa Szondy
Cells 2022, 11(8), 1333; https://doi.org/10.3390/cells11081333 - 13 Apr 2022
Cited by 3 | Viewed by 3065
Abstract
Skeletal muscle repair is initiated by local inflammation and involves the engulfment of dead cells (efferocytosis) by infiltrating macrophages at the injury site. Macrophages orchestrate the whole repair program, and efferocytosis is a key event not only for cell clearance but also for [...] Read more.
Skeletal muscle repair is initiated by local inflammation and involves the engulfment of dead cells (efferocytosis) by infiltrating macrophages at the injury site. Macrophages orchestrate the whole repair program, and efferocytosis is a key event not only for cell clearance but also for triggering the timed polarization of the inflammatory phenotype of macrophages into the healing one. While pro-inflammatory cytokines produced by the inflammatory macrophages induce satellite cell proliferation and differentiation into myoblasts, healing macrophages initiate the resolution of inflammation, angiogenesis, and extracellular matrix formation and drive myoblast fusion and myotube growth. Therefore, improper efferocytosis results in impaired muscle repair. Retinol saturase (RetSat) initiates the formation of various dihydroretinoids, a group of vitamin A derivatives that regulate transcription by activating retinoid receptors. Previous studies from our laboratory have shown that RetSat-null macrophages produce less milk fat globule-epidermal growth factor-factor-8 (MFG-E8), lack neuropeptide Y expression, and are characterized by impaired efferocytosis. Here, we investigated skeletal muscle repair in the tibialis anterior muscle of RetSat-null mice following cardiotoxin injury. Our data presented here demonstrate that, unexpectedly, several cell types participating in skeletal muscle regeneration compensate for the impaired macrophage functions, resulting in normal muscle repair in the RetSat-null mice. Full article
(This article belongs to the Special Issue Phagocytosis of Apoptotic Cells as Central Driver of the Resolution of Inflammation and the Restoration of Tissue Integrity)
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Review

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10 pages, 632 KiB  
Review
Efferocytosis during Skeletal Muscle Regeneration
by Gaëtan Juban and Bénédicte Chazaud
Cells 2021, 10(12), 3267; https://doi.org/10.3390/cells10123267 - 23 Nov 2021
Cited by 15 | Viewed by 5136
Abstract
Efferocytosis, i.e., engulfment of dead cells by macrophages, is a crucial step during tissue repair after an injury. Efferocytosis delineates the transition from the pro-inflammatory phase of the inflammatory response to the recovery phase that ensures tissue reconstruction. We present here the role [...] Read more.
Efferocytosis, i.e., engulfment of dead cells by macrophages, is a crucial step during tissue repair after an injury. Efferocytosis delineates the transition from the pro-inflammatory phase of the inflammatory response to the recovery phase that ensures tissue reconstruction. We present here the role of efferocytosis during skeletal muscle regeneration, which is a paradigm of sterile tissue injury followed by a complete regeneration. We present the molecular mechanisms that have been described to control this process, and particularly the metabolic control of efferocytosis during skeletal muscle regeneration. Full article
(This article belongs to the Special Issue Phagocytosis of Apoptotic Cells as Central Driver of the Resolution of Inflammation and the Restoration of Tissue Integrity)
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16 pages, 1955 KiB  
Review
Adipose Tissue Immunometabolism and Apoptotic Cell Clearance
by Tamás Röszer
Cells 2021, 10(9), 2288; https://doi.org/10.3390/cells10092288 - 2 Sep 2021
Cited by 15 | Viewed by 4815
Abstract
The safe removal of apoptotic debris by macrophages—often referred to as efferocytosis—is crucial for maintaining tissue integrity and preventing self-immunity or tissue damaging inflammation. Macrophages clear tissues of hazardous materials from dying cells and ultimately adopt a pro-resolving activation state. However, adipocyte apoptosis [...] Read more.
The safe removal of apoptotic debris by macrophages—often referred to as efferocytosis—is crucial for maintaining tissue integrity and preventing self-immunity or tissue damaging inflammation. Macrophages clear tissues of hazardous materials from dying cells and ultimately adopt a pro-resolving activation state. However, adipocyte apoptosis is an inflammation-generating process, and the removal of apoptotic adipocytes by so-called adipose tissue macrophages triggers a sequence of events that lead to meta-inflammation and obesity-associated metabolic diseases. Signals that allow apoptotic cells to control macrophage immune functions are complex and involve metabolites released by the apoptotic cells and also metabolites produced by the macrophages during the digestion of apoptotic cell contents. This review provides a concise summary of the adipocyte-derived metabolites that potentially control adipose tissue macrophage immune functions and, hence, may induce or alleviate adipose tissue inflammation. Full article
(This article belongs to the Special Issue Phagocytosis of Apoptotic Cells as Central Driver of the Resolution of Inflammation and the Restoration of Tissue Integrity)
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