Level C· Early human research exploring benefitsProspective StudyEurope PMCOpen access

Exosomes derived from a mesenchymal-like endometrial regenerative cells ameliorate renal ischemia reperfusion injury through delivery of CD73

Shao B., Wang HD., Ren SH., Chen Q., Wang ZB., Xu YN.

Prospective Study on Chronic Inflammation, published in Stem Cell Res Ther (2025) — summary generated from the PubMed abstract.

Open my reading list
Level C· Early human research exploring benefitsEvidence level of this study

Early human evidence such as case series or small samples is exploring possible benefits.

  • 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
Prospective Study
Journal
Stem Cell Res Ther (2025)
Reported sample size
—
Source database
Europe PMC
PMID
40140882
PMCID
PMC11948919
DOI
10.1186/s13287-025-04275-9
Citations
5

Abstract (original English)

Background Renal ischemia reperfusion (I/R) injury is a major contributor to graft dysfunction and inflammation leading to graft loss. The deregulation of purinergic signaling has been implicated in the pathogenesis of renal I/R injury. CD73 and the generation of adenosine during purine metabolism to protect against renal I/R injury. A mesenchymal-like endometrial regenerative cell (ERC) has demonstrated a significant therapeutic effect on renal I/R injury. CD73 is a phenotypic marker of human endometrial regenerative cell exosomes (ERC-Exo). However, its immunosuppressive function in regulating purinergic metabolism has been largely neglected. Here, we investigate the protective effects and mechanism of ERC-Exo against renal I/R injury. Methods Lentivirus-mediated CRISPR-Cas9 technology was employed to obtain CD73-specific knockout ERC-Exo (CD73 -/- ERC-Exo). C57BL/6 mice who underwent unilateral ureteral obstruction were divided into the Untreated, ERC-Exo-treated, and CD73 -/- ERC-Exo-treated groups. Renal function and pathological injury were assessed 3 days after renal reperfusion. The infiltration of CD4 + T cells and macrophages was analyzed by flow cytometry and immunofluorescence staining in kidneys. CD73-mediated immunosuppressive activity of ERC-Exo was investigated by bone marrow-derived macrophages (BMDM) co-culture assay in vitro. Flow cytometry determined macroph

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

How we grade evidence
EndometriumKidneyMacrophagesMesenchymal Stem CellsAnimalsMice, Inbred C57BLHumansMiceReperfusion Injury5'-Nucleotidase

Browse all related research

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

Related research