Autophagy of macrophages is regulated by PI3k/Akt/mTOR signalling in the development of diabetic encephalopathy

Wang, Beiyun; Zhong, Yuan; Li, Qinjie; Cui, Liang; Huang, Guangwen

doi:10.18632/aging.101586

Cited by 38 publications

(25 citation statements)

References 28 publications

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“…It has been demonstrated that PI3K/Akt/autophagy pathway is closely related to the regulation of cells migration and angiogenesis . The results also indicated the down‐regulation and up‐regulation of PI3K and Akt phosphorylation were found in EPCs with miR‐9‐5p mimics and inhibitor, respectively (Figure 5).…”

Section: Resultsmentioning

confidence: 86%

MiR‐9 promotes angiogenesis of endothelial progenitor cell to facilitate thrombi recanalization via targeting TRPM7 through PI3K/Akt/autophagy pathway

Zhou

Sun

Zhu

et al. 2020

J Cellular Molecular Medi

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Endothelial progenitor cells (EPCs) have emerged as a promising therapeutic choice for thrombi recanalization. However, this role of EPCs is confined by some detrimental factors. The aim of this study was to explore the role of the miR-9-5p in regulation of the proliferation, migration and angiogenesis of EPCs and the subsequent therapeutic role in thrombosis event. Wound healing, transwell assay, tube formation assay and in vivo angiogenesis assay were carried out to measure cell migration, invasion and angiogenic abilities, respectively. Western blot was performed to elucidate the relationship between miR-9-5p and TRPM7 in the autophagy pathway. It was found that miR-9-5p could promote migration, invasion and angiogenesis of EPCs by attenuating TRPM7 expression via activating PI3K/Akt/autophagy pathway. In conclusion, miR-9-5p, targets TRPM7 via the PI3K/Ak/autophagy pathway, thereby mediating cell proliferation, migration and angiogenesis in EPCs. Acting as a potential therapeutic target, miR-9-5p may play an important role in the prognosis of DVT.

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Section: Resultsmentioning

confidence: 86%

MiR‐9 promotes angiogenesis of endothelial progenitor cell to facilitate thrombi recanalization via targeting TRPM7 through PI3K/Akt/autophagy pathway

Zhou

Sun

Zhu

et al. 2020

J Cellular Molecular Medi

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“…Moreover, it is common knowledge that as an upstream pathway, the PI3K/Akt/mTOR signal is critical for the regulation of autophagy. [30, 31, 32] But the function of CaSR and PI3K/Akt/mTOR in HPASMCs of hypoxic cell models has not been discussed. In the current study, we first found that the inhibition of the PI3K/Akt/mTOR pathway is critical for the inhibition of hypoxia-induced autophagy by NPS2390.…”

Section: Discussionmentioning

confidence: 99%

NPS2390, a selective calcium-sensing receptor antagonist controls the phenotypic modulation of hypoxic human pulmonary arterial smooth muscle cells by regulating autophagy

Xue

Wei

et al. 2019

Journal of Translational Internal Medicine

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Background and Objectives Calcium-sensing receptor (CaSR) is known to regulate hypoxia-induced pulmonary hypertension (HPH) and vascular remodeling via the phenotypic modulation of pulmonary arterial smooth muscle cells (PASMCs) in small pulmonary arteries. Moreover, autophagy is an essential modulator of VSMC phenotype. But it is not clear whether CaSR can regulate autophagy involving the phenotypic modulation under hypoxia. Methods The viability of human PASMCs was detected by cell cycle and BrdU. The expressions of proliferation protein, phenotypic marker protein, and autophagy protein in human PASMCs were determined by western blot. Results Our results showed that hypoxia-induced autophagy was considerable at 24 h. The addition of NPS2390 decreased the expression of autophagy protein and synthetic phenotype marker protein osteopontin and increased the expression of contractile phenotype marker protein SMA-ɑ and calponin via suppressing downstream PI3K/Akt/mTOR signal pathways. Conclusions Our study demonstrates that treatment of NPS2390 was conducive to inhibit the proliferation and reverse phenotypic modulation of PASMCs by regulating autophagy levels.

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“…Homocysteine, an amino acid metabolite, regulates the connection between mTOR and lysosomal membranes and can inhibit autophagy through activating mTORC1 in vitro and in vivo [ 196 ]. PI3K/Akt/mTOR signaling regulated autophagy in macrophages in the development of diabetic encephalopathy and, in particular, chondrocytes by inhibiting miR-20 in osteoarthritis [ 44 , 45 ]. Curcumin, used in Indian and Chinese medicine as a wound-healing agent, among other uses, can also have a beneficial effect on osteoarthritis by possibly enhancing autophagy and reducing cell death and cartilage loss via Akt/mTOR signaling [ 197 ].…”

Section: Mtor Signalingmentioning

confidence: 99%

Key Signaling Pathways in Aging and Potential Interventions for Healthy Aging

Zhang

Wang

et al. 2021

Cells

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Aging is a fundamental biological process accompanied by a general decline in tissue function. Indeed, as the lifespan increases, age-related dysfunction, such as cognitive impairment or dementia, will become a growing public health issue. Aging is also a great risk factor for many age-related diseases. Nowadays, people want not only to live longer but also healthier. Therefore, there is a critical need in understanding the underlying cellular and molecular mechanisms regulating aging that will allow us to modify the aging process for healthy aging and alleviate age-related disease. Here, we reviewed the recent breakthroughs in the mechanistic understanding of biological aging, focusing on the adenosine monophosphate-activated kinase (AMPK), Sirtuin 1 (SIRT1) and mammalian target of rapamycin (mTOR) pathways, which are currently considered critical for aging. We also discussed how these proteins and pathways may potentially interact with each other to regulate aging. We further described how the knowledge of these pathways may lead to new interventions for antiaging and against age-related disease.

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Autophagy of macrophages is regulated by PI3k/Akt/mTOR signalling in the development of diabetic encephalopathy

Cited by 38 publications

References 28 publications

MiR‐9 promotes angiogenesis of endothelial progenitor cell to facilitate thrombi recanalization via targeting TRPM7 through PI3K/Akt/autophagy pathway

MiR‐9 promotes angiogenesis of endothelial progenitor cell to facilitate thrombi recanalization via targeting TRPM7 through PI3K/Akt/autophagy pathway

NPS2390, a selective calcium-sensing receptor antagonist controls the phenotypic modulation of hypoxic human pulmonary arterial smooth muscle cells by regulating autophagy

Key Signaling Pathways in Aging and Potential Interventions for Healthy Aging

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