Tissue-Specific, Disease-Signatured Macrophages in Control of Redox and Antioxidation in Metabolic Diseases

Topic Information

Dear Colleagues,

Reactive oxygen species (ROS) compose a complicated network signaling system, known as redox regulation, which is critical for maintenance of the homeostasis and metabolism of the human body. The imbalance of oxidation and anti-oxidation causes metabolic disorders, leading to many prevalent diseases, such as cancer, cardiovascular diseases, neurodegenerative diseases and diabetes. Macrophages play a pivotal role in immunity and nearly all physiological and pathological processes, during which macrophages act not only as one of the major target cells of oxidants, but also as important effector cells of inducible endogenous antioxidants. Accumulating evidence has demonstrated a pattern that macrophages dynamically adjust their activation profile toward a steadily changing microenvironment that requires altering their phenotype, a process known as macrophage polarization. Recent studies have shown that macrophage polarization is far more complicated than the classically catalogized proinflammatory M1 and anti-inflammatory M2, but more likely into a wide spectrum of phenotypes that do not fit rigidly into the definition of M1 or M2. To this end, studies on the tissue-specific, disease-signatured macrophage phenotypes appeared to be important for improving our understanding on the crosstalk between macrophages and microenvironment to regulate redox, metabolism, inflammation and immunity. After the outbreak of COVID-19, a notion arises that macrophages-associated regulation of ROS and immunity is altered by the viral infection and contributes to the disease progression and aggravation. The goal of this research topic aims to provide a scientific forum for the latest and innovative research for better understanding the role of macrophages as well as their specific polarization in the control of microenvironmental oxidative status that governs the initiation and progression of cancer, cardiovascular diseases, neurodegenerative diseases, diabetes and other related metabolic disorders. The scope of this research topic issue preferentially covers the latest and advanced results with innovative findings on the roles of macrophages, especially the specific phenotypic alteration of macrophages, in the control of microenvironmental oxidative status that governs the initiation and progression of cancer, cardiovascular diseases, neurodegenerative diseases, diabetes and other related metabolic disorders. Both research and review articles are welcome except case reports.

Dr. Xiangwei Xiao
Dr. Yingmei Feng
Dr. Zhiyong Lei
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Antioxidants antioxidants	6.0	10.6	2012	16.9 Days	CHF 2900	Submit
Biomolecules biomolecules	4.8	9.4	2011	18.4 Days	CHF 2700	Submit
Journal of Cardiovascular Development and Disease jcdd	2.4	2.6	2014	25.7 Days	CHF 2700	Submit
Metabolites metabolites	3.5	5.7	2011	16.1 Days	CHF 2700	Submit
Neurology International neurolint	3.2	3.7	2009	26.5 Days	CHF 1600	Submit
Pharmaceutics pharmaceutics	4.9	7.9	2009	15.5 Days	CHF 2900	Submit

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Published Papers (2 papers)

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All Antioxidants Biomolecules JCDD Metabolites Neurology International Pharmaceutics

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Open AccessArticle

Low Fluoride Regulates Macrophage Polarization Through Mitochondrial Autophagy Mediated by PINK1/Parkin Axis

by Fengyu Xie, Jing Zhou, Bingshu Liu, Lijun Zhao, Cunqi Lv, Qiong Zhang, Lin Yuan, Dianjun Sun and Wei Wei

Biomolecules 2025, 15(5), 647; https://doi.org/10.3390/biom15050647 - 30 Apr 2025

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Abstract

Fluoride exposure has been shown to affect immune cell subsets and immune function, but its impact on macrophage polarization remains unclear. This study investigates the effects of low fluoride exposure on macrophage polarization and its underlying mechanisms through epidemiological surveys, animal experiments, and [...] Read more.

Fluoride exposure has been shown to affect immune cell subsets and immune function, but its impact on macrophage polarization remains unclear. This study investigates the effects of low fluoride exposure on macrophage polarization and its underlying mechanisms through epidemiological surveys, animal experiments, and in vitro cell experiments. In the population-based epidemiological survey, we used mass cytometry to assess the impact of low fluoride exposure (0.570–2.027 mg/L) in the environment on human immune cell populations following the current water improvement and fluoride reduction measures. A rat fluorosis model was established by treating rats with sodium fluoride (NaF) in drinking water at concentrations of 0 mg/L, 5 mg/L, 10 mg/L, 25 mg/L, and 50 mg/L for 90 days., and morphological changes were assessed by hematoxylin–eosin (H&E) staining and transmission electron microscopy in the spleen of rats. Flow cytometry was used to analyze the proportion of macrophage subtypes in the spleen, while Western blot and immunofluorescence were performed to detect the expression of mitochondrial autophagy-related proteins. An M1 macrophage model was constructed in vitro by inducing THP-1 cells, and the effects of fluoride on macrophage-related cell markers and cytokines were assessed using flow cytometry and ELISA, respectively, following intervention with an autophagy inhibitor. Mitochondrial membrane potential and mitochondrial–lysosomal colocalization are analyzed through flow cytometry and confocal microscopy. The study aims to investigate the role of mitophagy in sodium fluoride-induced macrophage polarization. Epidemiological investigations revealed that low fluoride increases the proportion of blood monocytes, as well as the expression levels of CD68 (a macrophage surface marker), CD86 (an M1 macrophage marker), and the inflammatory cytokine IFN-γ in peripheral blood mononuclear cells (PBMCs). In the rats of NaF-treated groups, splenic tissues exhibited inflammatory infiltration, mitochondrial swelling, and increased autophagosome formation. Moreover, low fluoride activated the PINK1/Parkin-mediated mitophagy pathway, promoting an increase in the M2/M1 macrophage ratio. In vitro experiments further confirmed that autophagy inhibitors reversed the NaF-induced increase in the M2/M1 macrophage ratio. This study demonstrates that low fluoride induces inflammatory responses in the body and drives M1 macrophage polarization toward M2 macrophages via mitophagy. These findings highlight the potential immunological risks associated with low fluoride and provide mechanistic insights into the interplay among fluoride, mitophagy, and macrophage polarization. Full article

(This article belongs to the Topic Tissue-Specific, Disease-Signatured Macrophages in Control of Redox and Antioxidation in Metabolic Diseases)

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Open AccessArticle

Lactiplantibacillus plantarum and Saussurea costus as Therapeutic Agents against a Diabetic Rat Model—Approaches to Investigate Pharmacophore Modeling of Human IkB Kinase and Molecular Interaction with Dehydrocostus Lactone of Saussurea costus

by Metab A. AlGeffari, Dina Mansour, Omar Ahmed-Farid, Einas Mohamed Yousef, Shereen A. Mohamed, Mahmoud M. A. Moustafa, Hassan Barakat and Khalid Abd El Ghany

Metabolites 2023, 13(6), 764; https://doi.org/10.3390/metabo13060764 - 19 Jun 2023

Cited by 3 | Viewed by 2562

Abstract

Lactic acid bacteria is well-known as a vital strategy to alleviate or prevent diabetes. Similarly, the plant Saussurea costus (Falc) Lipsch is a preventive power against diabetes. Here, we aimed to determine whether lactic acid bacteria or Saussurea costus is more effective in [...] Read more.

Lactic acid bacteria is well-known as a vital strategy to alleviate or prevent diabetes. Similarly, the plant Saussurea costus (Falc) Lipsch is a preventive power against diabetes. Here, we aimed to determine whether lactic acid bacteria or Saussurea costus is more effective in treating a diabetic rat model in a comparative study manner. An in vivo experiment was conducted to test the therapeutic activity of Lactiplantibacillus plantarum (MW719476.1) and S. costus plants against an alloxan-induced diabetic rat model. Molecular, biochemical, and histological analyses were investigated to evaluate the therapeutic characteristics of different treatments. The high dose of S. costus revealed the best downregulated expression for the IKBKB, IKBKG, NfkB1, IL-17A, IL-6, IL-17F, IL-1β, TNF-α, TRAF6, and MAPK genes compared to Lactiplantibacillus plantarum and the control groups. The downregulation of IKBKB by S. costus could be attributed to dehydrocostus lactone as an active compound with proposed antidiabetic activity. So, we performed another pharmacophore modeling analysis to test the possible interaction between human IkB kinase beta protein and dehydrocostus lactone as an antidiabetic drug. Molecular docking and MD simulation data confirmed the interaction between human IkB kinase beta protein and dehydrocostus lactone as a possible drug. The target genes are important in regulating type 2 diabetes mellitus signaling, lipid and atherosclerosis signaling, NF-κB signaling, and IL-17 signaling pathways. In conclusion, the S. costus plant could be a promising source of novel therapeutic agents for treating diabetes and its complications. Dehydrocostus lactone caused the ameliorative effect of S. costus by its interaction with human IkB kinase beta protein. Further, future studies could be conducted to find the clinical efficacy of dehydrocostus lactone. Full article

(This article belongs to the Topic Tissue-Specific, Disease-Signatured Macrophages in Control of Redox and Antioxidation in Metabolic Diseases)

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