Resolution of Inflammation after Skeletal Muscle Ischemia–Reperfusion Injury: A Focus on the Lipid Mediators Lipoxins, Resolvins, Protectins and Maresins

Skeletal muscle ischemia reperfusion is very frequent in humans and results not only in muscle destruction but also in multi-organ failure and death via systemic effects related to inflammation and oxidative stress. In addition to overabundance of pro-inflammatory stimuli, excessive and uncontrolled...

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Vydané v:Antioxidants Ročník 11; číslo 6; s. 1213
Hlavní autori: Barnig, Cindy, Lutzweiler, Gaetan, Giannini, Margherita, Lejay, Anne, Charles, Anne-Laure, Meyer, Alain, Geny, Bernard
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: Basel MDPI AG 20.06.2022
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Abstract Skeletal muscle ischemia reperfusion is very frequent in humans and results not only in muscle destruction but also in multi-organ failure and death via systemic effects related to inflammation and oxidative stress. In addition to overabundance of pro-inflammatory stimuli, excessive and uncontrolled inflammation can also result from defects in resolution signaling. Importantly, the resolution of inflammation is an active process also based on specific lipid mediators including lipoxins, resolvins and maresins that orchestrate the potential return to tissue homeostasis. Thus, lipid mediators have received growing attention since they dampen deleterious effects related to ischemia–reperfusion. For instance, the treatment of skeletal muscles with resolvins prior to ischemia decreases polymorphonuclear leukocyte (PMN) infiltration. Additionally, remote alterations in lungs or kidneys are reduced when enhancing lipid mediators’ functions. Accordingly, lipoxins prevented oxidative-stress-mediated tissue injuries, macrophage polarization was modified and in mice lacking DRV2 receptors, ischemia/reperfusion resulted in excessive leukocyte accumulation. In this review, we first aimed to describe the inflammatory response during ischemia and reperfusion in skeletal muscle and then discuss recent discoveries in resolution pathways. We focused on the role of specialized pro-resolving mediators (SPMs) derived from polyunsaturated fatty acids (PUFAs) and their potential therapeutic applications.
AbstractList Skeletal muscle ischemia reperfusion is very frequent in humans and results not only in muscle destruction but also in multi-organ failure and death via systemic effects related to inflammation and oxidative stress. In addition to overabundance of pro-inflammatory stimuli, excessive and uncontrolled inflammation can also result from defects in resolution signaling. Importantly, the resolution of inflammation is an active process also based on specific lipid mediators including lipoxins, resolvins and maresins that orchestrate the potential return to tissue homeostasis. Thus, lipid mediators have received growing attention since they dampen deleterious effects related to ischemia–reperfusion. For instance, the treatment of skeletal muscles with resolvins prior to ischemia decreases polymorphonuclear leukocyte (PMN) infiltration. Additionally, remote alterations in lungs or kidneys are reduced when enhancing lipid mediators’ functions. Accordingly, lipoxins prevented oxidative-stress-mediated tissue injuries, macrophage polarization was modified and in mice lacking DRV2 receptors, ischemia/reperfusion resulted in excessive leukocyte accumulation. In this review, we first aimed to describe the inflammatory response during ischemia and reperfusion in skeletal muscle and then discuss recent discoveries in resolution pathways. We focused on the role of specialized pro-resolving mediators (SPMs) derived from polyunsaturated fatty acids (PUFAs) and their potential therapeutic applications.
Skeletal muscle ischemia reperfusion is very frequent in humans and results not only in muscle destruction but also in multi-organ failure and death via systemic effects related to inflammation and oxidative stress. In addition to overabundance of pro-inflammatory stimuli, excessive and uncontrolled inflammation can also result from defects in resolution signaling. Importantly, the resolution of inflammation is an active process also based on specific lipid mediators including lipoxins, resolvins and maresins that orchestrate the potential return to tissue homeostasis. Thus, lipid mediators have received growing attention since they dampen deleterious effects related to ischemia-reperfusion. For instance, the treatment of skeletal muscles with resolvins prior to ischemia decreases polymorphonuclear leukocyte (PMN) infiltration. Additionally, remote alterations in lungs or kidneys are reduced when enhancing lipid mediators' functions. Accordingly, lipoxins prevented oxidative-stress-mediated tissue injuries, macrophage polarization was modified and in mice lacking DRV2 receptors, ischemia/reperfusion resulted in excessive leukocyte accumulation. In this review, we first aimed to describe the inflammatory response during ischemia and reperfusion in skeletal muscle and then discuss recent discoveries in resolution pathways. We focused on the role of specialized pro-resolving mediators (SPMs) derived from polyunsaturated fatty acids (PUFAs) and their potential therapeutic applications.Skeletal muscle ischemia reperfusion is very frequent in humans and results not only in muscle destruction but also in multi-organ failure and death via systemic effects related to inflammation and oxidative stress. In addition to overabundance of pro-inflammatory stimuli, excessive and uncontrolled inflammation can also result from defects in resolution signaling. Importantly, the resolution of inflammation is an active process also based on specific lipid mediators including lipoxins, resolvins and maresins that orchestrate the potential return to tissue homeostasis. Thus, lipid mediators have received growing attention since they dampen deleterious effects related to ischemia-reperfusion. For instance, the treatment of skeletal muscles with resolvins prior to ischemia decreases polymorphonuclear leukocyte (PMN) infiltration. Additionally, remote alterations in lungs or kidneys are reduced when enhancing lipid mediators' functions. Accordingly, lipoxins prevented oxidative-stress-mediated tissue injuries, macrophage polarization was modified and in mice lacking DRV2 receptors, ischemia/reperfusion resulted in excessive leukocyte accumulation. In this review, we first aimed to describe the inflammatory response during ischemia and reperfusion in skeletal muscle and then discuss recent discoveries in resolution pathways. We focused on the role of specialized pro-resolving mediators (SPMs) derived from polyunsaturated fatty acids (PUFAs) and their potential therapeutic applications.
Author Meyer, Alain
Lejay, Anne
Giannini, Margherita
Barnig, Cindy
Charles, Anne-Laure
Geny, Bernard
Lutzweiler, Gaetan
AuthorAffiliation 4 Department of Chest Diseases, University Hospital of Besançon, 25030 Besançon, France
2 Physiology and Functional Exploration Service, University Hospital of Strasbourg, 1 Place de l’Hôpital, 67091 Strasbourg, France
1 Team 3072 “Mitochondria, Oxidative Stress and Muscle Protection”, Translational Medicine Federation of Strasbourg (FMTS), Faculty of Medicine, University of Strasbourg, 11 Rue Humann, 67000 Strasbourg, France; cbarnig@chu-besancon.fr (C.B.); margherita.giannini@chru-strasbourg.fr (M.G.); anne.lejay@chru-strasbourg.fr (A.L.); anne.laure.charles@unistra.fr (A.-L.C.); alain.meyer1@chru-strasbourg.fr (A.M.)
3 INSERM, EFS BFC, UMR1098, Interactions Hôte-Greffon-Tumeur/Ingénierie Cellulaire et Génique, University Bourgogne Franche-Comté, LabEx LipSTIC, 25000 Besançon, France
5 Laboratoire de Polymères, Biopolymères et Surfaces (PBS), Université de Rouen Normandie, 55 Rue Saint-Germain, 27000 Evreux, France; gaetanlutzweiler@gmail.com
AuthorAffiliation_xml – name: 1 Team 3072 “Mitochondria, Oxidative Stress and Muscle Protection”, Translational Medicine Federation of Strasbourg (FMTS), Faculty of Medicine, University of Strasbourg, 11 Rue Humann, 67000 Strasbourg, France; cbarnig@chu-besancon.fr (C.B.); margherita.giannini@chru-strasbourg.fr (M.G.); anne.lejay@chru-strasbourg.fr (A.L.); anne.laure.charles@unistra.fr (A.-L.C.); alain.meyer1@chru-strasbourg.fr (A.M.)
– name: 5 Laboratoire de Polymères, Biopolymères et Surfaces (PBS), Université de Rouen Normandie, 55 Rue Saint-Germain, 27000 Evreux, France; gaetanlutzweiler@gmail.com
– name: 4 Department of Chest Diseases, University Hospital of Besançon, 25030 Besançon, France
– name: 2 Physiology and Functional Exploration Service, University Hospital of Strasbourg, 1 Place de l’Hôpital, 67091 Strasbourg, France
– name: 3 INSERM, EFS BFC, UMR1098, Interactions Hôte-Greffon-Tumeur/Ingénierie Cellulaire et Génique, University Bourgogne Franche-Comté, LabEx LipSTIC, 25000 Besançon, France
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Snippet Skeletal muscle ischemia reperfusion is very frequent in humans and results not only in muscle destruction but also in multi-organ failure and death via...
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StartPage 1213
SubjectTerms Antioxidants
Apoptosis
Chemokines
Cytokines
death
Dehydrogenases
Heparan sulfate
Homeostasis
Inflammation
Ischemia
Kidneys
Kinases
leukocytes
Leukocytes (polymorphonuclear)
lipid mediators
Lipid peroxidation
Lipids
lipoxin
Macrophages
Metabolism
Microorganisms
Mitochondria
Mitochondrial DNA
Multiple organ dysfunction syndrome
muscles
Musculoskeletal system
Neutrophils
Oxidative stress
Peptides
Permeability
Physiology
Polyunsaturated fatty acids
protectins and maresins
Proteins
Reperfusion
resolvins
Review
Signal transduction
Skeletal muscle
Therapeutic applications
therapeutics
Tumor necrosis factor-TNF
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Title Resolution of Inflammation after Skeletal Muscle Ischemia–Reperfusion Injury: A Focus on the Lipid Mediators Lipoxins, Resolvins, Protectins and Maresins
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