ArticleStem cell research & therapy2022
The role of the aging microenvironment on the fate of PDGFRβ lineage cells in skeletal muscle repair.
Article in Stem cell research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 12 citations in OpenAlex.
- Multifunctional PDGF Nanofiber and MnCe Nanozyme-Incorporated Composite Hydrogel for Enhanced Skeletal Muscle Regeneration.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- Macrophage regulation of extracellular matrix remodeling in aging skeletal muscle.Ageing research reviews · 2026Review
- Overactive PDGFRα and PDGFRβ promote distinct phenotypes of skeletal muscle fibrosis and stiffness, with PDGFRβ also driving muscle growth.American journal of physiology. Cell physiology · 2026Article
- PDGFRβ signaling restrains myocyte function to limit the regenerative capacity of skeletal muscle.The Journal of clinical investigation · 2026Article
- Overactive PDGFRα and PDGFRβ promote distinct yet overlapping phenotypes of skeletal muscle fibrosis and stiffness, with PDGFRβ also driving drastic muscle growth.bioRxiv : the preprint server for biology · 2026Article
- Surface marker-defined functional subpopulations of mesenchymal stromal cells: mechanisms, applications, and clinical translation.Frontiers in bioengineering and biotechnology · 2026Review
- SMAD7: riding on fibrosis-limiting routes and beyond.EMBO molecular medicine · 2025Review
- Nicotinamide and Pyridoxine in Muscle Aging: Nutritional Regulation of Redox, Inflammation, and Regeneration.Antioxidants (Basel, Switzerland) · 2025Review
- Restoration of skeletal muscle function via mesenchymal stem cells: mechanistic insights and therapeutic advances in myasthenia gravis.Frontiers in cell and developmental biology · 2025Review
- Suppressing PDGFRβ Signaling Enhances Myocyte Fusion to Promote Skeletal Muscle Regeneration.bioRxiv : the preprint server for biology · 2024Article
- Cancerous Conditions Accelerate the Aging of Skeletal Muscle via Mitochondrial DNA Damage.International journal of molecular sciences · 2024Article
- Endothelial-specific telomerase inactivation causes telomere-independent cell senescence and multi-organ dysfunction characteristic of aging.Aging cell · 2024Article
- Lineage tracing reveals a novel PDGFRβScientific reports · 2024Article
- Intermuscular adipose tissue in obesity and related disorders: cellular origins, biological characteristics and regulatory mechanisms.Frontiers in endocrinology · 2023Review
- Senescence induces fundamental changes in the secretome of mesenchymal stromal cells (MSCs): implications for the therapeutic use of MSCs and their derivates.Frontiers in bioengineering and biotechnology · 2023Review
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundDuring aging, perturbation of muscle progenitor cell (MPC) constituents leads to progressive loss of muscle mass and accumulation of adipose and fibrotic tissue. Mesenchymal stem cells (MSCs) give rise to adipocytes and fibroblasts that accumulate in injured and pathological skeletal muscle through constitutive activation of platelet-derived growth factor receptors (PDGFRs). Although the role of the PDGFRα has been widely explored, there is a paucity of evidence demonstrating the role of PDGFRβ in aged skeletal muscle.
methodsIn this study, we investigated the role of PDGFRβ lineage cells in skeletal muscle during aging by using Cre/loxP lineage tracing technology. The PDGFR-Cre mice were crossed with global double-fluorescent Cre reporter mice (mTmG) that indelibly marks PDGFRβ lineage cells. Those cells were analyzed and compared at different ages in the skeletal muscle of the mice.
resultsOur results demonstrated that PDGFRβ lineage cells isolated from the muscles of young mice are MPC-like cells that exhibited satellite cell morphology, expressed Pax7, and undergo myogenic differentiation producing myosin heavy chain expressing myotubes. Conversely, the PDGFRβ lineage cells isolated from muscles of old mice displayed MSC morphology with a reduced myogenic differentiation potential while expressing adipogenic and fibrotic differentiation markers. PDGFRβ lineage cells also gave rise to newly regenerated muscle fibers in young mice after muscle injury, but their muscle regenerative process is reduced in old mice.
conclusionsOur data suggest that PDGFRβ lineage cells function as MPCs in young mice, while the same PDGFRβ lineage cells from old mice undergo a fate switch participating in adipose and fibrotic tissue infiltration in aged muscle. The inhibition of fate-switching in PDGFRβ lineage cells may represent a potential approach to prevent fibrosis and fatty infiltration in skeletal muscle during the aging process.
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