Clinical-grade human umbilical cord-derived mesenchymal stem cells improved skeletal muscle dysfunction in age-associated sarcopenia mice

Wang, Chao; Zhao, Bichun; Zhai, Jinglei; Wang, Ailin; Cao, Ning; Liao, Tuling; Su, Ruyu; He, Lijuan; Li, Yanhua; Pei, Xuetao; Jia, Yi; Yue, Wen

doi:10.1038/s41419-023-05843-8

Cited by 9 publications

(5 citation statements)

References 71 publications

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“… 8 , 9 , 23 This hypothesis is not corroborated by our observation of scattered MHC-II+ cells not preferentially associated with LC3+ or p62+ puncta. In addition, fast-twitching type II myofibers are mostly affected by impaired autophagy, 24 but could better survive increased activation of autophagy. The primary limitation of our study is the heterogeneous single cases of exceptionally rare neuromyophaties analyzed and, hence static morphologic assessment of autophagy instead of appropriate dynamic flux analysis.…”

Section: Discussionmentioning

confidence: 99%

Autophagy increase in Merosin-Deficient Congenital Muscular Dystrophy type 1A

et al. 2023

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The autophagy process recycles dysfunctional cellular components and protein aggregates by sequestering them in autophagosomes directed to lysosomes for enzymatic degradation. A basal level of autophagy is essential for skeletal muscle maintenance. Increased autophagy occurs in several forms of muscular dystrophy and in the merosin-deficient congenital muscular dystrophy 1A mouse model (dy3k/dy3k) lacking the laminin-α2 chain. This pilot study aimed to compare autophagy marker expression and autophagosomes presence using light and electron microscopes and western blotting in diagnostic muscle biopsies from newborns affected by different congenital muscular myopathies and dystrophies. Morphological examination showed dystrophic muscle features, predominance of type 2A myofibers, accumulation of autophagosomes in the subsarcolemmal areas, increased number of autophagosomes overexpressing LC3b, Beclin-1 and ATG5, in the merosin-deficient newborn suggesting an increased autophagy. In Duchenne muscular dystrophy, nemaline myopathy, and spinal muscular atrophy the predominant accumulation of p62+ puncta rather suggests an autophagy impairment.

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Section: Discussionmentioning

confidence: 99%

Autophagy increase in Merosin-Deficient Congenital Muscular Dystrophy type 1A

et al. 2023

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“…On a different note, an innovative study by Wang et al [119] has revealed the potential of clinical-grade human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) in two models of age-related sarcopenia mice. hUC-MSC transplantation was noted to restore skeletal muscle strength and performance through the cells' roles in enhancing the expression of extracellular matrix proteins, activating satellite cells, enhancing autophagy, and impeding cellular aging.…”

Section: Stem Cell Therapiesmentioning

confidence: 99%

Emerging Therapeutic Strategies in Sarcopenia: An Updated Review on Pathogenesis and Treatment Advances

Najm,

Niculescu,

Grumezescu

et al. 2024

IJMS

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Sarcopenia is a prevalent degenerative skeletal muscle condition in the elderly population, posing a tremendous burden on diseased individuals and healthcare systems worldwide. Conventionally, sarcopenia is currently managed through nutritional interventions, physical therapy, and lifestyle modification, with no pharmaceutical agents being approved for specific use in this disease. As the pathogenesis of sarcopenia is still poorly understood and there is no treatment recognized as universally effective, recent research efforts have been directed at better comprehending this illness and diversifying treatment strategies. In this respect, this paper overviews the new advances in sarcopenia treatment in correlation with its underlying mechanisms. Specifically, this review creates an updated framework for sarcopenia, describing its etiology, pathogenesis, risk factors, and conventional treatments, further discussing emerging therapeutic approaches like new drug formulations, drug delivery systems, stem cell therapies, and tissue-engineered scaffolds in more detail.

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“…In order to investigate NMJ degeneration in relation to the onset of sarcopenia, a well-accepted sarcopenic animal model, SAMP8 against its control strain, SAMR1 without sarcopenia phenotype were used in this study (Wang et al, 2023). In SAMP8, grip strength peaked at 8 months and decreased significantly by 32.00% at 10 months (p < 0.001).…”

Section: Samp8 Was Validated As Sarcopenic Animal Model With Samr1 As...mentioning

confidence: 99%

Prevention of age‐related neuromuscular junction degeneration in sarcopenia by low‐magnitude high‐frequency vibration

Bao,

Cui,

Liu

et al. 2024

Aging Cell

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Neuromuscular junction (NMJ) degeneration is one of pathological factors of sarcopenia. Low‐magnitude high‐frequency vibration (LMHFV) was reported effective in alleviating the sarcopenia progress. However, no previous study has investigated treatment effects of LMHFV targeting NMJ degeneration in sarcopenia. We first compared morphological differences of NMJ between sarcopenic and non‐sarcopenic subjects, as well as young and old C57BL/6 mice. We then systematically characterized the age‐related degeneration of NMJ in SAMP8 against its control strain, SAMR1 mice, from 3 to 12 months old. We also investigated effects of LMHFV in SAMP8 on the maintenance of NMJ during the onset of sarcopenia with respect to the Agrin‐LRP4‐MuSK‐Dok7 pathway and investigated the mechanism related to ERK1/2 signaling. We observed sarcopenic/old NMJ presented increased acetylcholine receptors (AChRs) cluster fragmentation and discontinuity than non‐sarcopenic/young NMJ. In SAMP8, NMJ degeneration (morphologically at 6 months and functionally at 8 months) was observed associated with the sarcopenia onset (10 months). SAMR1 showed improved NMJ morphology and function compared with SAMP8 at 10 months. Skeletal muscle performance was improved at Month 4 post‐LMHFV treatment. Vibration group presented improved NMJ function at Months 2 and 6 posttreatment, accompanied with alleviated morphological degeneration at Month 4 posttreatment. LMHFV increased Dok7 expression at Month 4 posttreatment. In vitro, LMHFV could promote AChRs clustering in myotubes by increasing Dok7 expression through suppressing ERK1/2 phosphorylation. In conclusion, NMJ degeneration was observed associated with the sarcopenia onset in SAMP8. LMHFV may attenuate NMJ degeneration and sarcopenia progression by increasing Dok7 expression through suppressing ERK1/2 phosphorylation.

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Clinical-grade human umbilical cord-derived mesenchymal stem cells improved skeletal muscle dysfunction in age-associated sarcopenia mice

Cited by 9 publications

References 71 publications

Autophagy increase in Merosin-Deficient Congenital Muscular Dystrophy type 1A

Autophagy increase in Merosin-Deficient Congenital Muscular Dystrophy type 1A

Emerging Therapeutic Strategies in Sarcopenia: An Updated Review on Pathogenesis and Treatment Advances

Prevention of age‐related neuromuscular junction degeneration in sarcopenia by low‐magnitude high‐frequency vibration

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