Level D· Scientific groundwork from lab and animal studiesAnimal StudyPubMedOpen access

Ror2 signaling regulated by differential Wnt proteins determines pathological fate of muscle mesenchymal progenitors.

Kamizaki K., Katsukawa M., Yamamoto A., Fukada SI., Uezumi A., Endo M.

Animal Study, published in Cell Death Dis (2024) — summary generated from the PubMed abstract.

Open my reading list
Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
Cell Death Dis (2024)
Country
England
Reported sample size
—
Source database
PubMed
PMID
39468010
PMCID
PMC11519583
DOI
10.1038/s41419-024-07173-9
Citations
4

Abstract (original English)

Skeletal muscle mesenchymal progenitors (MPs) play a critical role in supporting muscle regeneration. However, under pathological conditions, they contribute to intramuscular adipose tissue accumulation, involved in muscle diseases, including muscular dystrophy and sarcopenia, age-related muscular atrophy. How MP fate is determined in these different contexts remains unelucidated. Here, we report that Ror2, a non-canonical Wnt signaling receptor, is selectively expressed in MPs and regulates their pathological features in a differential ligand-dependent manner. We identified Wnt11 and Wnt5b as ligands of Ror2. In vitro, Wnt11 inhibited MP senescence, which is required for normal muscle regeneration, and Wnt5b promoted MP proliferation. We further found that both Wnts are abundant in degenerating muscle and synergistically stimulate Ror2, leading to unwanted MP proliferation and eventually intramuscular adipose tissue accumulation. These findings provide evidence that Ror2-mediated signaling elicited by differential Wnts plays a critical role in determining the pathological fate of MPs.

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
Receptor Tyrosine Kinase-like Orphan ReceptorsAnimalsMesenchymal Stem CellsMiceMuscle, SkeletalWnt ProteinsCell ProliferationHumansMice, Inbred C57BLSignal Transduction

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.