Level B· Emerging clinical evidence with positive signalsClinical TrialPubMed

Adipose stem-cell-derived microvesicles ameliorate long-term bladder ischemia-induced bladder underactivity.

Chiang BJ., Mao SH., Chen TS., Chung SD., Chien CT.

Clinical Trial, published in J Formos Med Assoc (2024) — summary generated from the PubMed abstract.

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Level B· Emerging clinical evidence with positive signalsEvidence level of this study

Several human studies show positive signals, while research methods and sample sizes continue to develop.

  • 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
Clinical Trial
Journal
J Formos Med Assoc (2024)
Country
Singapore
Reported sample size
—
Source database
PubMed
PMID
39658414
DOI
10.1016/j.jfma.2024.12.006
Citations
1

Abstract (original English)

Background/purpose The mechanism for long-term hypoxia/ischemia induced bladder underactivity is uncertain. It requires an effectively therapeutic treatment. Therefore, we determined the pathophysiologic mechanisms of long-term bilateral partial iliac arterial occlusion (BPAO)-induced bladder underactivity and explored the therapeutic potential of adipose-derived stem cells (ADSCs) and ADSC-derived microvesicles (MVs) on BPAO-induced bladder dysfunction. Methods The study included four groups: sham, BPAO, BPAO + ADSCs, and BPAO + ADSC-MVs. ADSCs or ADSC-MVs were isolated, characterized with specific CD markers and injected through the femoral artery to the rat bladders. Real-time laser speckle contrast imaging evaluated bladder microcirculation after BPAO. The transcystometrogram, pelvic nerve activity, bladder histology, immunohistochemistry, and lipid peroxidation assays were conducted after 4-week BPAO induction. The molecular mechanisms of bladder expression of purinergic P2X2/P2X3 and cholinergic M2/M3 receptors for regulating bladder contractility, nerve growth factor (NGF) for nerve injury repair, and collagen-1 for fibrosis were evaluated. Results Long-term BPAO significantly reduced bladder microcirculation, prolonged the intercontraction interval, decreased voiding volume, increased residual urine volume, lengthened phase 1 contraction, shortened phase 2 contraction,

What this study does not prove

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

Evidence level

Several human studies show positive signals, while research methods and sample sizes continue to develop.

How we grade evidence
AnimalsRatsUrinary BladderIschemiaRats, Sprague-DawleyCell-Derived MicroparticlesAdipose TissueDisease Models, AnimalFemaleMale

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