Muscular dystrophies (MDs) are a heterogeneous group of genetic diseases caused by mutations in proteins that mainly constitute the sarcolemma and the cytosol of the muscle fibers. Under physiological conditions, inflammation is fundamental to guide tissue recovery following injury: innate immune cells, mostly macrophages, eliminate cellular debris, maintain muscle homeostasis, and regulate muscular regeneration through the secretion of several factors that regulate the proliferation of the satellite cells. In MDs the genetic defects determine chronic injuries in muscular tissues so that the inflammation – and all the pathogenic pathways that are related to inflammatory events – are up-regulated throughout the entire life of affected individuals. Even if in MDs inflammation is a shared feature, differences exist in molecules, pathways involved, and in cellular infiltrates, suggesting a specific pathogenic mechanism accounting for each form of MDs.
The development of pathological phenotypes of muscular dystrophies depends on earlier processes such as aberrant intracellular calcium homeostasis, altered ROS metabolism and mytophagy, leading to uncontrolled recruitment of inflammatory cells in muscular tissues. The goal of this topic is to describe the multiple interactions among the inflammatory immune cells and the other muscle-resident stem cells driving necrosis, autophagy, fat infiltration and, as a final step, fibrosis. We welcome submissions of Original Research articles and Reviews covering the following themes:
Preclinical and clinical research into the cellular and molecular mediators of inflammation resolution in muscular dystrophies
• Elucidate inflammation resolution pathways and promising targets for biomarkers or therapy in muscular dystrophy
• Current knowledge and data in inflammation resolution to understand and improve the management of patients affected by muscular dystrophy
Muscular dystrophies (MDs) are a heterogeneous group of genetic diseases caused by mutations in proteins that mainly constitute the sarcolemma and the cytosol of the muscle fibers. Under physiological conditions, inflammation is fundamental to guide tissue recovery following injury: innate immune cells, mostly macrophages, eliminate cellular debris, maintain muscle homeostasis, and regulate muscular regeneration through the secretion of several factors that regulate the proliferation of the satellite cells. In MDs the genetic defects determine chronic injuries in muscular tissues so that the inflammation – and all the pathogenic pathways that are related to inflammatory events – are up-regulated throughout the entire life of affected individuals. Even if in MDs inflammation is a shared feature, differences exist in molecules, pathways involved, and in cellular infiltrates, suggesting a specific pathogenic mechanism accounting for each form of MDs.
The development of pathological phenotypes of muscular dystrophies depends on earlier processes such as aberrant intracellular calcium homeostasis, altered ROS metabolism and mytophagy, leading to uncontrolled recruitment of inflammatory cells in muscular tissues. The goal of this topic is to describe the multiple interactions among the inflammatory immune cells and the other muscle-resident stem cells driving necrosis, autophagy, fat infiltration and, as a final step, fibrosis. We welcome submissions of Original Research articles and Reviews covering the following themes:
Preclinical and clinical research into the cellular and molecular mediators of inflammation resolution in muscular dystrophies
• Elucidate inflammation resolution pathways and promising targets for biomarkers or therapy in muscular dystrophy
• Current knowledge and data in inflammation resolution to understand and improve the management of patients affected by muscular dystrophy
