Epigenetic dysregulation in aged muscle stem cells drives mesenchymal progenitor expansion via IL-6 and Spp1 signaling.

Giulia Riparini, Morgan Mackenzie, Faiza Naz, Stephen Brooks, Kan Jiang, Anshu Deewan, Brittany Dulek, Shamima Islam, Kyung Dae Ko, Wanxia L Tsai, Massimo Gadina, Stefania Dell'Orso, Vittorio Sartorelli

Laboratory of Muscle Stem Cells and Gene Regulation, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, USA.Laboratory of Muscle Stem Cells and Gene Regulation, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, USA. · pubmed

Paper

Abstract

Sarcopenia, the age-related decline in muscle mass, strength and function, is characterized by impaired muscle homeostasis, reduced regenerative potential of muscle stem cells (MuSCs) and increased fibrosis. Here we report that aged MuSCs can autonomously instruct fibro-adipogenic progenitors (FAPs) to proliferate and acquire a fibrogenic phenotype, independent of other cell types. Both the polycomb-deficient Ezh2

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Research summary

Aged muscle stem cells drive the proliferation of fibro-adipogenic progenitors through IL-6 and Spp1 signaling. This research addresses the mechanisms underlying muscle degeneration in aging, which is a critical aspect of longevity and age-related decline.

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