ArticleNature communications2021
Resolvin-D2 targets myogenic cells and improves muscle regeneration in Duchenne muscular dystrophy.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 74 citations in OpenAlex.
- Resolvin E1 promotes the resolution of inflammation and enhances myogenic responses during aged skeletal muscle regeneration.GeroScience · 2026Article
- Downstream Pathways of Dystrophin Deficiency in Duchenne Muscular Dystrophy: Implications for Muscle Degeneration and Regeneration.Journal of cachexia, sarcopenia and muscle · 2026Review
- Fibroadipogenic progenitor-secreted prostaglandin E2 coordinates stem cell fate via autocrine and paracrine crosstalk in healthy and dystrophic muscle.Cell death and differentiation · 2026Article
- Long-chain Polyunsaturated Fatty Acids MitigatebioRxiv : the preprint server for biology · 2026Article
- Elucidation of a potent pro-resolving mediator of inflammation resolution via human neutrophil-vascular endothelial cell interactions.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Lipoxin A4 activates Nrf2 expression and mitigates hyperglycaemia-induced impairment of myogenesis and rescues damage to mitochondria.Journal of physiology and biochemistry · 2026Article
- From lipid switch to tissue repair: how resolvins reprogram macrophage polarization and function.Immunometabolism (Cobham, Surrey) · 2026Review
- Co-culture of bone marrow-derived macrophages with aged primary myoblasts.Biology methods & protocols · 2026Article
- Skeletal muscle disuse atrophy: protection by omega-3 polyunsaturated fatty acids.NFS journal · 2025Article
- Reprogramming inflammation: Mechanisms and therapeutic targeting of eicosanoids and pro-resolving mediators.European journal of pharmacology · 2025Review
- Bioactive lipid mediator class switching regulates myogenic cell progression and muscle regeneration.Nature communications · 2025Article
- Lipid droplets as cell fate determinants in skeletal muscle.Trends in endocrinology and metabolism: TEM · 2025Review
- Resolvin D2 and Its Effects on the Intestinal Mucosa of Crohn's Disease Patients: A Promising Immune Modulation Therapeutic Target.International journal of molecular sciences · 2025Article
- Functional Foods, a Hope to Delay Muscle Dystrophy Progression: A Potential Role for Omega Fatty Acids.Nutrients · 2025Review
- FNDC1 is a myokine that promotes myogenesis and muscle regeneration.The EMBO journal · 2025Article
- Scientific and Technological Prospecting on Polymeric Particles Containing Extracellular Matrix Peptides for the Treatment of Duchenne Muscular Dystrophy.Recent advances in drug delivery and formulation · 2025Review
- Transcriptomic and lipidomic profiling reveals distinct bioactive lipid signatures in slow and fast muscles and highlights the role of resolvin-D2 in fiber type determination during myogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- A potent proresolving mediator 17R-resolvin D2 from human macrophages, monocytes, and saliva.Science advances · 2024Article
- Low-dose pro-resolving mediators temporally reset the resolution response to microbial inflammation.Molecular medicine (Cambridge, Mass.) · 2024Article
- A Novel MAO-B/SSAO Inhibitor Improves Multiple Aspects of Dystrophic Phenotype inAntioxidants (Basel, Switzerland) · 2024Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Lack of dystrophin causes muscle degeneration, which is exacerbated by chronic inflammation and reduced regenerative capacity of muscle stem cells in Duchenne Muscular Dystrophy (DMD). To date, glucocorticoids remain the gold standard for the treatment of DMD. These drugs are able to slow down the progression of the disease and increase lifespan by dampening the chronic and excessive inflammatory process; however, they also have numerous harmful side effects that hamper their therapeutic potential. Here, we investigated Resolvin-D2 as a new therapeutic alternative having the potential to target multiple key features contributing to the disease progression. Our in vitro findings showed that Resolvin-D2 promotes the switch of macrophages toward their anti-inflammatory phenotype and increases their secretion of pro-myogenic factors. Moreover, Resolvin-D2 directly targets myogenic cells and promotes their differentiation and the expansion of the pool of myogenic progenitor cells leading to increased myogenesis. These effects are ablated when the receptor Gpr18 is knocked-out, knocked-down, or blocked by the pharmacological antagonist O-1918. Using different mouse models of DMD, we showed that Resolvin-D2 targets both inflammation and myogenesis leading to enhanced muscle function compared to glucocorticoids. Overall, this preclinical study has identified a new therapeutic approach that is more potent than the gold-standard treatment for DMD.
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