Activation of autophagy mediated by PI3K/Akt/mTOR signalling cascade alleviates impaired adipose-derived stem cell osteogenesis in a diabetic microenvironment.
Lou F., Fu T., Li Q., Rao P., Peng S., Lu S.
Animal Study, published in Br J Pharmacol (2025) — summary generated from the PubMed abstract.
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
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
- Br J Pharmacol (2025)
- Country
- England
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 40170369
- DOI
- 10.1111/bph.70016
- Citations
- 5
Abstract (original English)
Background and purpose Advanced glycation end products (AGEs) contribute to the onset and advancement of diabetic osteoporosis (DOP). Adipose-derived stem cells (ASCs) have garnered attention in the field of bone renewal; the mechanisms leading to decreased osteogenesis within a diabetic environment are not fully understood. This study explores the effects/molecular pathways of AGEs on the osteogenesis of ASCs both in vitro and in vivo. Experimental approach A DOP mouse model was used, and ASCs were extracted from the inguinal fat of C57BL/6 mice. ASCs were cultivated in an osteogenic differentiation medium and were exposed to AGEs, Torin1 (an autophagy activator), or ibandronate (IBAN), a PI3K/Akt/mTOR signalling inhibitor. Osteogenesis and autophagy activity were measured. Key results The expression of osteogenic markers, OPN and RUNX2, was decreased, ALP activities were impaired, and the formation of mineralised nodules was reduced in ASCs treated with AGEs. Additionally, the autophagic flux was blocked, and there was an increase in PI3K/Akt/mTOR signalling markers. After treatment with Torin1, the osteogenesis of ASCs in a diabetic microenvironment was restored by activating autophagy. Moreover, in the AGEs and DOP model, treatment with IBAN up-regulated autophagy and rescued the impaired osteogenesis of ASCs in diabetic microenvironment. Conclusion and implications AGEs de
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.
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