Abstract
In healthy subjects, homeostasis and repair of skeletal muscle rely on muscle-resident and circulating stem and progenitor cells, i.e., satellite cells and bone marrow–derived hematopoietic and endothelial (CPCs) or mesenchymal stem and progenitor cells (MPCs). Mature endothelial cells (ECs) support myogenesis by growth factor secretion [1]. Myotonic dystrophy type 1 (MD1) is a multisystem disorder of genetic origin that causes muscle wasting and impaired muscle regeneration. Furthermore, patients with MD1 are more prone to become adipose [2]. Muscle regeneration in obese MD1 patients by circulating precursor and supporting cells might be hampered since obesity suppresses the number and function of circulating precursor cells, as already shown for endothelial progenitor cells (EPCs) [3]. Weight loss management by bariatric surgery in obese patients without MD1 elevated the number of EPCs [4]. In MD1, however, bariatric surgery–induced CPC, MPC, and EC number increases could be...
| Originalsprache | Englisch |
|---|---|
| Zeitschrift | Obesity Surgery |
| Jahrgang | 29 |
| Ausgabenummer | 1 |
| Seiten (von - bis) | 311-315 |
| Seitenumfang | 5 |
| ISSN | 0960-8923 |
| DOIs | |
| Publikationsstatus | Veröffentlicht - 15.01.2019 |
Fördermittel
Funding The study was funded by the eSwiss Medical and Surgical Center in St. Gallen and ETH Zurich, Switzerland.
UN SDGs
Dieser Output leistet einen Beitrag zu folgendem(n) Ziel(en) für nachhaltige Entwicklung
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SDG 3 – Gesundheit und Wohlergehen
Strategische Forschungsbereiche und Zentren
- Forschungsschwerpunkt: Gehirn, Hormone, Verhalten - Center for Brain, Behavior and Metabolism (CBBM)
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