Astragaloside IV — mediated endothelial progenitor cell exosomes promote autophagy and inhibit apoptosis in hyperglycemic damaged endothelial cells via miR-21/PTEN axis

Xiong, Wu; Huang, Xin-ling; Wang, Xiaoliang; Lan, Hong-wei; Wang, Tingting; Chen, Zilin; Yang, Qian-pei; Hu, Ai-lin; Xia, Yang; Zhou, Zhong-zhi

doi:10.5603/fhc.a2022.0030

Cited by 6 publications

(1 citation statement)

References 31 publications

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“…Regulating the PI3K/AKT/mTOR signaling pathway to activate autophagy is an effective way to reduce DM-related EC injury. For example, miR-126, miR-199a-3p, and exosome miR-21 upregulate the expression of autophagy-promoting genes, such as ATG5, Beclin1, and LC3, by inhibiting the PI3K/AKT/mTOR signaling pathway; activate EC autophagy; restore autophagy flux; and alleviate endothelial injury induced by glycolipid metabolism disorders ( 81 – 84 ). Furthermore, in diabetic mice, activating promyelocytic leukemia zinc finger protein (PLZF) can upregulate PI3K expression, promote EC autophagy, and protect the vascular endothelium from AGE-induced injury ( 85 ).…”

Section: Mechanism Of Autophagy Regulating Vascular Endothelial Injur...mentioning

confidence: 99%

Physiological and pathological characteristics of vascular endothelial injury in diabetes and the regulatory mechanism of autophagy

et al. 2023

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Vascular endothelial injury in diabetes mellitus (DM) is the major cause of vascular disease, which is closely related to the occurrence and development of a series of vascular complications and has a serious negative impact on a patient’s health and quality of life. The primary function of normal vascular endothelium is to function as a barrier function. However, in the presence of DM, glucose and lipid metabolism disorders, insulin resistance, inflammatory reactions, oxidative stress, and other factors cause vascular endothelial injury, leading to vascular endothelial lesions from morphology to function. Recently, numerous studies have found that autophagy plays a vital role in regulating the progression of vascular endothelial injury. Therefore, this article compares the morphology and function of normal and diabetic vascular endothelium and focuses on the current regulatory mechanisms and the important role of autophagy in diabetic vascular endothelial injury caused by different signal pathways. We aim to provide some references for future research on the mechanism of vascular endothelial injury in DM, investigate autophagy’s protective or injurious effect, and study potential drugs using autophagy as a target.

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Section: Mechanism Of Autophagy Regulating Vascular Endothelial Injur...mentioning

confidence: 99%

Physiological and pathological characteristics of vascular endothelial injury in diabetes and the regulatory mechanism of autophagy

et al. 2023

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Astragaloside promotes the secretion of MSC-derived exosomal miR-146a-5p by regulating TRAF6/NF-κB pathway to attenuate inflammation in high glucose-impaired endothelial cells

Chen,

et al. 2024

In Vitro Cell.Dev.Biol.-Animal

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Mechanism of Astragaloside IV in Treatment of Renal Tubulointerstitial Fibrosis

Wang,

Luan,

Guo

2024

Chin. J. Integr. Med.

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Astragaloside IV — mediated endothelial progenitor cell exosomes promote autophagy and inhibit apoptosis in hyperglycemic damaged endothelial cells via miR-21/PTEN axis

Abstract: This article has been peer reviewed and published immediately upon acceptance.It is an open access article, which means that it can be downloaded, printed, and distributed freely, provided the work is properly cited. Articles in "Folia Histochemica et Cytobiologica" are listed in PubMed.

Cited by 6 publications

References 31 publications

Physiological and pathological characteristics of vascular endothelial injury in diabetes and the regulatory mechanism of autophagy

Physiological and pathological characteristics of vascular endothelial injury in diabetes and the regulatory mechanism of autophagy

Astragaloside promotes the secretion of MSC-derived exosomal miR-146a-5p by regulating TRAF6/NF-κB pathway to attenuate inflammation in high glucose-impaired endothelial cells

Mechanism of Astragaloside IV in Treatment of Renal Tubulointerstitial Fibrosis

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