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Metabolic Inflammation: Signaling Pathway and Molecular Mechanisms

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 January 2019) | Viewed by 11852

Special Issue Editors

Department of Neuroscience “Rita Levi Montalcini”, University of Turin, 10125 Turin, Italy
Interests: metabolic inflammation; NLRP3 inflammasome; diet-induced metabolic diseases; advanced glycation and products
Special Issues, Collections and Topics in MDPI journals
Department of Biomedical Sciences and Human Oncology−Pharmacology Section, Medical School–University of Bari “Aldo Moro”, Bari, Italy
Interests: endothelial dysfunction; endothelial mediators; insulin signaling; oxidative stress; metabolic syndrome; adipocytokines
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The role of chronic, low-grade inflammation, recently referred to as “metaflammation”, in altering metabolism is increasingly being accepted. Metaflammation can complicate the clinical features of cardiovascular diseases by causing an energetic imbalance towards catabolism and interfering with homeostatic signalling, thus leading to the development of cardio-metabolic diseases (CMD), multifactorial diseases that continue to rise in prevalence, mainly in Western countries, with important health and economic implications. Besides, metaflammation may represent biological phenomena that are able to couple impairment in metabolic processes with the development of cancer and neurodegenerative disorders. Clinical trials suggest that modulating inflammation prevents CMD, but studies that explore its effects on other chronic and noncommunicable diseases are scarce and controversial, and the identification of selective mechanisms of cross-talk between metaflammation and diseases development is far from clear. There is therefore an increasing need to better understand molecular mechanisms of progression in CMD, as well as in other chronic pathological conditions, to develop novel treatments that target specifically these mechanisms and can slow disease progression. This Special Issue is trying to address these goals by publishing articles that describe both novel molecular pathways implicated in metaflammation and novel treatment ideas. We hope that the papers collected here may offer readers improved knowledge of innovative and original advances that have been made in pathogenesis and the management of CMD, as well as other metaflammation-related clinical conditions.

Prof. Dr. Massimo Collino
Prof. Dr. Monica Montagnani
Guest Editors

Manuscript Submission Information

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Keywords

  • nutrition
  • metabolic inflammation
  • inflammatory pathways
  • insulin resistance
  • endothelial dysfunction
  • perivascular adipose tissue
  • cardio-metabolic diseases
  • diet-related organ dysfunctions

Published Papers (2 papers)

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13 pages, 654 KiB  
Article
Comparison of Fatty Acid Profiles in a Group of Female Patients with Chronic Kidney Diseases (CKD) and Metabolic Syndrome (MetS)–Similar Trends of Changes, Different Pathophysiology
by Małgorzata Szczuko, Małgorzata Kaczkan, Arleta Drozd, Dominika Maciejewska, Joanna Palma, Anna Owczarzak, Natalia Marczuk, Przemysław Rutkowski and Sylwia Małgorzewicz
Int. J. Mol. Sci. 2019, 20(7), 1719; https://doi.org/10.3390/ijms20071719 - 06 Apr 2019
Cited by 21 | Viewed by 4258
Abstract
Fatty acid (FA) profiles in the plasma of patients with metabolic syndrome and chronic kidney disease (CKD) seem to be identical despite their different etiology (dietary mistakes vs. cachexia). The aim of this study was to compare both profiles and to highlight the [...] Read more.
Fatty acid (FA) profiles in the plasma of patients with metabolic syndrome and chronic kidney disease (CKD) seem to be identical despite their different etiology (dietary mistakes vs. cachexia). The aim of this study was to compare both profiles and to highlight the differences that could influence the improvement of the treatment of patients in both groups. The study involved 73 women, including 24 patients with chronic kidney disease treated with haemodialysis, 19 patients with metabolic syndrome (MetS), and 30 healthy women in the control group. A total of 35 fatty acids and derivatives were identified and quantified by gas chromatography. Intensified elongation processes from acid C10:0 to C16:0 were noted in both groups (more intense in MetS), as well as an increased synthesis of arachidonic acid (C20:4n6), which was more intense in CKD. Significant correlations of oleic acid (C18:1n9), gamma linoleic acid (C18:3n6), and docosatetraenoate acid (C22:4n6) with parameters of CKD patients were observed. In the MetS group, auxiliary metabolic pathways of oleic acid were activated, which simultaneously inhibited the synthesis of eicosapentanoic acid (EPA) and docosahexaenoic acid (DHA) from alpha lipoic acid (ALA). On the other hand, in the group of female patients with CKD, the synthesis of EPA and DHA was intensified. Activation of the synthesis of oleic acid (C18: 1n9 ct) and trans-vaccinic acid (C18:1) is a protective mechanism in kidney diseases and especially in MetS due to the increased concentration of saturated fatty acid (SFA) in plasma. The cause of the increased amount of all FAs in plasma in the CKD group, especially in the case of palmitic (C16:0) and derivatives stearic (C18:0) acids, may be the decomposition of adipose tissue and the progressing devastation of the organism, whereas, in the MetS group, dietary intake seems to be the main reason for the increase in SFA. Moreover, in MetS, auxiliary metabolic pathways are activated for oleic acid, which cause the simultaneous inhibition of EPA and DHA synthesis from ALA, whereas, in the CKD group, we observe an increased synthesis of EPA and DHA. The higher increase of nervonic acid (C24:1) in CKD suggests a higher degree of demyelination and loss of axons. Full article
(This article belongs to the Special Issue Metabolic Inflammation: Signaling Pathway and Molecular Mechanisms)
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25 pages, 1530 KiB  
Review
Exosome and Macrophage Crosstalk in Sleep-Disordered Breathing-Induced Metabolic Dysfunction
by Abdelnaby Khalyfa, Leila Kheirandish-Gozal and David Gozal
Int. J. Mol. Sci. 2018, 19(11), 3383; https://doi.org/10.3390/ijms19113383 - 29 Oct 2018
Cited by 38 | Viewed by 7150
Abstract
Obstructive sleep apnea (OSA) is a highly prevalent worldwide public health problem that is characterized by repetitive upper airway collapse leading to intermittent hypoxia, pronounced negative intrathoracic pressures, and recurrent arousals resulting in sleep fragmentation. Obesity is a major risk factor of OSA [...] Read more.
Obstructive sleep apnea (OSA) is a highly prevalent worldwide public health problem that is characterized by repetitive upper airway collapse leading to intermittent hypoxia, pronounced negative intrathoracic pressures, and recurrent arousals resulting in sleep fragmentation. Obesity is a major risk factor of OSA and both of these two closely intertwined conditions result in increased sympathetic activity, oxidative stress, and chronic low-grade inflammation, which ultimately contribute, among other morbidities, to metabolic dysfunction, as reflected by visceral white adipose tissue (VWAT) insulin resistance (IR). Circulating extracellular vesicles (EVs), including exosomes, are released by most cell types and their cargos vary greatly and reflect underlying changes in cellular homeostasis. Thus, exosomes can provide insights into how cells and systems cope with physiological perturbations by virtue of the identity and abundance of miRNAs, mRNAs, proteins, and lipids that are packaged in the EVs cargo, and are secreted from the cells into bodily fluids under normal as well as diseased states. Accordingly, exosomes represent a novel pathway via which a cohort of biomolecules can travel long distances and result in the modulation of gene expression in selected and targeted recipient cells. For example, exosomes secreted from macrophages play a critical role in innate immunity and also initiate the adaptive immune response within specific metabolic tissues such as VWAT. Under normal conditions, phagocyte-derived exosomes represent a large portion of circulating EVs in blood, and carry a protective signature against IR that is altered when secreting cells are exposed to altered physiological conditions such as those elicited by OSA, leading to emergence of IR within VWAT compartment. Consequently, increased understanding of exosome biogenesis and biology should lead to development of new diagnostic biomarker assays and personalized therapeutic approaches. Here, the evidence on the major biological functions of macrophages and exosomes as pathophysiological effectors of OSA-induced metabolic dysfunction is discussed. Full article
(This article belongs to the Special Issue Metabolic Inflammation: Signaling Pathway and Molecular Mechanisms)
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