Effects of rapamycin and OSI-027 on α-SMA in lung tissue of SD rat pups with hyperoxic lung injury

Liang, Mulin; Dang, Hongxing; Li, Qinghe; Huang, Weiben; Liu, Chengjun

doi:10.1016/j.bbrc.2021.02.061

Cited by 3 publications

(2 citation statements)

References 15 publications

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“…OSI'nin faz 1 çalışmasında 43 hasta tedavi edilmiş, DST olarak ejeksiyon fraksiyonunda azalma, yan etki olarak anoreksiya ve bulantı görülmüştür. Biri kolorektal kanseri, diğeri parotis kanseri olan iki hastada tümörde küçülme izlenmiştir 43 .…”

Section: Mtor Kinaz Inhibitörleriunclassified

Targeted Cancer Therapy: PI3K/Akt/mTOR Inhibitors

Küpeli

2022

Arşiv Kaynak Tarama Dergisi

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Cancers generally contain multiple genetic and epigenetic abnormalities, but several key genes maintain the malignant phenotype and cellular survival. The PI3K/Akt/mTOR pathway is a central signaling system that plays a role in many important physiological events. Since the PI3K/Akt/mTOR pathway is used by many tumor types, it is thought that inhibitors used against this pathway may have a wide therapeutic efficacy. Significant response rates could not be obtained in phase 1 studies with any of the agents in monotherapy, and other options are being investigated by administering high doses in short periods and combining drugs that may affect different pathways.

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Section: Mtor Kinaz Inhibitörleriunclassified

Targeted Cancer Therapy: PI3K/Akt/mTOR Inhibitors

Küpeli

2022

Arşiv Kaynak Tarama Dergisi

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“…Morita et al reported that mTOR regulates the expression of mitochondrial fission process 1, controlling mitochondrial dynamics and cell survival [25]. Additionally, the expression of α-SMA in hyperoxic lung injury has been shown to be increased via activation of the mTOR signaling pathway [26]. In healthy dental pulp, the expression of α-SMA is confined to blood vessels.…”

Section: Introductionmentioning

confidence: 99%

Role of alpha smooth muscle actin in odontogenic differentiation of dental pulp stem cells

Ma,

Shen,

et al. 2023

European J Oral Sciences

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Pulpotomy is an effective treatment for retaining vital pulp after pulp exposure caused by caries removal and/or trauma. The expression of alpha smooth muscle actin (α‐SMA) is increased during the wound‐healing process, and α‐SMA‐positive fibroblasts accelerate tissue repair. However, it remains largely unknown whether α‐SMA‐positive fibroblasts influence pulpal repair. In this study, we established an experimental rat pulpotomy model and found that the expression of α‐SMA was increased in dental pulp after pulpotomy relative to that in normal dental pulp. In vitro results showed that the expression of α‐SMA was increased during the induction of odontogenic differentiation in dental pulp stem cells (DPSCs) compared with untreated DPSCs. Moreover, α‐SMA overexpression promoted the odontogenic differentiation of DPSCs via increasing mitochondrial function. Mechanistically, α‐SMA overexpression activated the mammalian target of rapamycin (mTOR) signaling pathway. Inhibition of the mTOR signaling pathway by rapamycin decreased the mitochondrial function in α‐SMA‐overexpressing DPSCs and suppressed the odontogenic differentiation of DPSCs. Furthermore, we found that α‐SMA overexpression increased the secretion of transforming growth factor beta‐1 (TGF‐β1). In sum, our present study demonstrates a novel mechanism by which α‐SMA promotes odontogenic differentiation of DPSCs by increasing mitochondrial respiratory activity via the mTOR signaling pathway.

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