RETRACTED ARTICLE: Exosomes derived from bone mesenchymal stem cells attenuate myocardial fibrosis both in vivo and in vitro via autophagy activation: the key role of miR-199a-3p/mTOR pathway

Fan, Chenrong; Wang, Qizeng; Chen, Youjin; Ye, Tingting; Fan, Yuncao

doi:10.1007/s13577-022-00680-x

Cited by 6 publications

(3 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Most studies focused on activating proliferation related signaling pathways and inhibiting apoptosis related factors in cardiomyocytes and endothelial cells, while less attention was paid to the molecular mechanism of MSC-Exos on the immune system and fibroblasts. Recent studies have shown that non coding RNA in MSC-Exos inhibits mTOR in fibroblasts (Fan et al, 2022), while MSC-Exo activates mTOR related signaling pathways in cardiomyocytes (Wang et al, 2017). In addition to the traditional AKT/PI3K signaling pathway and the NF-κB related signaling pathway, recent studies have shown that non-coding RNA in BMSC-Exos inhibits iron death in cardiomyocytes through Pum2/PRDX6 single pathway.…”

Section: Discussionmentioning

confidence: 99%

“…Inhibiting miR-199a-3p in DOX-induced cardiomyocytes effectively reversed the effects of MSC-Exos, downregulating survivin (Lee et al, 2021). In another study, Fan et al found that fibrotic cardiomyocyte autophagy was also promoted by miR-199a-3p in BMSC-Exos by inhibiting mTOR, thereby reducing cardiac fibrosis (Fan et al, 2022).…”

Section: Protective Effect Of Mirna In Cardiac Injurymentioning

confidence: 98%

See 1 more Smart Citation

Mesenchymal stem cell-derived exosomes: a possible therapeutic strategy for repairing heart injuries

Zhu

Fan

et al. 2023

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Mesenchymal stem cells (MSCs) are one of the most potent therapeutic strategies for repairing cardiac injury. It has been shown in the latest studies that MSCs cannot survive in the heart for a long time. Consequently, the exosomes secreted by MSCs may dominate the repair of heart injury and promote the restoration of cardiac cells, vascular proliferation, immune regulation, etc. Based on the current research, the progress of the acting mechanism, application prospects and challenges of exosomes, including non-coding RNA, in repairing cardiac injuries are summarised in this article.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Protective Effect Of Mirna In Cardiac Injurymentioning

confidence: 98%

Mesenchymal stem cell-derived exosomes: a possible therapeutic strategy for repairing heart injuries

Zhu

Fan

et al. 2023

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

show abstract

“…This inhibition effectively elevates autophagic flux, including the levels of Beclin1 and LC3 II. Previous studies have indicated that some microRNAs induce autophagy by inhibiting mTOR [ 42 , 43 ]. Recent studies have also shown that tRF3008A suppresses the progression and metastasis of colorectal cancer by destabilizing FOXK1 in an AGO-dependent manner [ 9 ], while tRF-3001b aggravates the development of nonalcoholic fatty liver disease by inhibiting autophagy via the same mechanism [ 44 ].…”

Section: Discussionmentioning

confidence: 99%

tRNA-Derived Fragment tRF-5009A Regulates Autophagy and Degeneration of Cartilage in Osteoarthritis via Targeting mTOR

Deng

Long

Liu

et al. 2022

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

tRNA-derived fragments (tRFs) have been reported to have critical regulatory roles in osteoarthritis (OA). Recent studies have suggested that autophagy promotes the homeostasis of the extracellular matrix of chondrocytes in OA. However, the role of tRFs in posttranscriptional gene regulation during autophagy in OA is unknown. Therefore, we explored the role of tRF-5009A in the posttranscriptional gene regulation of autophagy and cartilage degeneration in OA. Using RNA sequencing, we identified tRF-5009A, the tRNAValCAC-derived fragment, in OA tissues and explored its expression by quantitative reverse transcription PCR and fluorescence in situ hybridization. We further investigated the relationship between the expression of tRF-5009A and clinical factors in OA. Chondrocytes were transfected with a tRF-5009A inhibitor or mimic to determine their functions, including in relation to autophagy and the cartilage phenotype. A rescue experiment and dual-luciferase reporter assay were conducted to determine whether the 3 ′ -untranslated region (UTR) of mTOR contains a tRF-5009A-binding site. tRF-5009A was downregulated in the cartilage of OA knees, especially in damaged areas. mTOR was highly expressed in damaged cartilage and negatively correlated with the expression of tRF-5009A; transfection with a tRF-5009A inhibitor promoted the expression of mTOR and suppressed autophagy, whereas transfection with a tRF-5009A mimic had the opposite effect. A dual-luciferase reporter assay showed that tRF-5009A silenced the expression of mTOR by binding to its 3 ′ -UTR. Thus, tRF-5009A regulates autophagy and cartilage degeneration in OA by targeting mTOR. In summary, these findings provide an additional tool for the clinical diagnosis and novel targeted therapy of OA.

show abstract

BMSC-derived Exosomes Ameliorate Peritoneal Dialysis-associated Peritoneal Fibrosis via the Mir-27a-3p/TP53 Pathway

Zhao,

Zhan

et al. 2024

CURR MED SCI

View full text Add to dashboard Cite

RETRACTED ARTICLE: Exosomes derived from bone mesenchymal stem cells attenuate myocardial fibrosis both in vivo and in vitro via autophagy activation: the key role of miR-199a-3p/mTOR pathway

Cited by 6 publications

References 39 publications

Mesenchymal stem cell-derived exosomes: a possible therapeutic strategy for repairing heart injuries

Mesenchymal stem cell-derived exosomes: a possible therapeutic strategy for repairing heart injuries

tRNA-Derived Fragment tRF-5009A Regulates Autophagy and Degeneration of Cartilage in Osteoarthritis via Targeting mTOR

BMSC-derived Exosomes Ameliorate Peritoneal Dialysis-associated Peritoneal Fibrosis via the Mir-27a-3p/TP53 Pathway

Contact Info

Product

Resources

About