Sulforaphane protects human umbilical vein endothelial cells from oxidative stress via the miR‑34a/SIRT1 axis by upregulating nuclear factor erythroid‑2‑related factor 2

Li, Tao; Pang, Qian; Liu, Yongbin; Bai, Ming; Yu, Peng; Zhang, Zheng

doi:10.3892/etm.2021.9617

Cited by 14 publications

(10 citation statements)

References 50 publications

(54 reference statements)

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“…SirT1 sirna was used to detect the potential mechanisms of SFn in H 2 o 2 -stimulated apoptotic chondrocytes. consistent with previous studies, rna interference against SirT1 suppressed SFn-mediated inhibition of the anti-apoptosis effect (61,62). expression levels of SirT1 were suppressed whereas levels of cleaved caspase-3 were significantly elevated in the SIRT1 siRNA transfection group.…”

Section: Discussionsupporting

confidence: 92%

Sulforaphane protects against oxidative stress‑induced apoptosis via activating SIRT1 in mouse osteoarthritis

Chen

Huang

et al. 2021

Mol Med Rep

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osteoarthritis (oa), the most common form of human joint disease, is characterized by progressive degeneration of the articular cartilage, synovitis and subchondral osteoporosis. chondrocyte apoptosis is the primary pathogenic mechanism of oa and is considered to be a potential therapeutic target. Sulforaphane (SFn), a dietary isothiocyanate obtained from cruciferous vegetables, has been reported to exert an anti-apoptotic effect by activating sirtuin 1 (SirT1). To the best of our knowledge, however, the effects of SFn on apoptotic responses in oa have not been reported. in the present study, SFN was shown to significantly inhibit chondrocyte apoptosis while enhancing expression levels of SirT1 in a H 2 o 2 -induced oa mouse model. The anti-apoptotic effect of SFn was reversed by SirT1 small interfering rna, implying that SirT1 exerted a protective role against the effect of SFn on chondrocytes. The expression levels of c/eBP homologous protein, 78-kda glucose regulated protein, Bax, Bcl-2 and cleaved caspase 3 were found to be downregulated in SFn-treated mice. Furthermore, SFn ameliorated cartilage degradation in the OA mouse model. These findings indicate that SFn exerted an anti-apoptotic effect on chondrocytes and ameliorated oa in vivo by activating the SirT1 signaling pathway.

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Section: Discussionsupporting

confidence: 92%

Sulforaphane protects against oxidative stress‑induced apoptosis via activating SIRT1 in mouse osteoarthritis

Chen

Huang

et al. 2021

Mol Med Rep

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“…Overexpression of miR-34a enhanced radiationinduced oxidative stress in cardiomyocyte, while macrophage migration inhibition reduced cellular reactive oxygen species (ROS) through the miR-34a/SIRT1 signaling pathway (48). More importantly, inhibition of miR-34a mitigated oxidative stress induced by H 2 O 2 to protect vascular endothelial cells by targeting SIRT1 (49). The role of inflammation in MIRI is still controversial.…”

Section: Mir-34a and Cardiovascular Oxidative Stress And Inflammationmentioning

confidence: 99%

Targeting the microRNA-34a as a Novel Therapeutic Strategy for Cardiovascular Diseases

Hua

Liu

Liang³

et al. 2022

Front. Cardiovasc. Med.

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Cardiovascular diseases (CVDs) are still the main cause of morbidity and mortality worldwide and include a group of disorders varying from vasculature, myocardium, arrhythmias and cardiac development. MicroRNAs (miRs) are endogenous non-coding RNAs with 18–23 nucleotides that regulate gene expression. The miR-34 family, including miR-34a/b/c, plays a vital role in the regulation of myocardial physiology and pathophysiological processes. Recently, miR-34a has been implicated in cardiovascular fibrosis, dysfunction and related cardiovascular disorders as an essential regulator. Interestingly, there is a pivotal link among miR-34a, cardiovascular fibrosis, and Smad4/TGF-β1 signaling. Notably, both loss-of-function and gain-of-function approaches identified the critical roles of miR-34a in cardiovascular apoptosis, autophagy, inflammation, senescence and remodeling by modulating multifunctional signaling pathways. In this article, we focus on the current understanding of miR-34a in biogenesis, its biological effects and its implications for cardiac pathologies including myocardial infarction, heart failure, ischaemia reperfusion injury, cardiomyopathy, atherosclerosis, hypertension and atrial fibrillation. Thus, further understanding of the effects of miR-34a on cardiovascular diseases will aid the development of effective interventions. Targeting for miR-34a has emerged as a potential therapeutic target for cardiovascular dysfunction and related diseases.

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“…The prolonged exposure of saturated fatty acids to MIN6 β-cells and pancreatic islets increased the expression of miR-34a ( Lovis et al, 2008 ). Furthermore, miR-34a leads to endothelial dysfunction and vascular senescence in diabetes ( Li et al, 2016 ; Carracedo et al, 2019 ; Thounaojam and Bartoli, 2019 ), increasing the overall risk of oxidative stress and inflammation with or without diabetes ( Li et al, 2016 ; Cheleschi et al, 2019 ; Xiong et al, 2019 ; Zimta et al, 2019 ; Li et al, 2021 ; Mahjabeen et al, 2021 ; Zhu et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Functional role of miR-34a in diabetes and frailty

et al. 2022

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Emerging evidence has shown that microRNAs (miRNAs) play critical role in the pathogenesis of several disorders. In the present minireview, we focus our attention on the functional role of a specific miRNA, namely miR-34a, in the pathophysiology of frailty and diabetes mellitus. Based on the current literature, we speculate that this miRNA may serve as a potential biomarker of frailty in diabetic older adults. Additionally, its actions on oxidative stress might represent a druggable target to obtain new potentials treatments.

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Sulforaphane protects human umbilical vein endothelial cells from oxidative stress via the miR‑34a/SIRT1 axis by upregulating nuclear factor erythroid‑2‑related factor 2

Cited by 14 publications

References 50 publications

Sulforaphane protects against oxidative stress‑induced apoptosis via activating SIRT1 in mouse osteoarthritis

Sulforaphane protects against oxidative stress‑induced apoptosis via activating SIRT1 in mouse osteoarthritis

Targeting the microRNA-34a as a Novel Therapeutic Strategy for Cardiovascular Diseases

Functional role of miR-34a in diabetes and frailty

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