Resveratrol Ameliorated Vascular Calcification by Regulating Sirt-1 and Nrf2

Zhang, P.; Li, Y.; Du, Yifei; Li, G.; Wang, L.; Zhou, Fachun

doi:10.1016/j.transproceed.2016.10.023

Cited by 72 publications

(64 citation statements)

References 29 publications

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“…This result is consistent with in vivo data showing that sulfide protects myocytes from oxidative stress [13] and that it protects vascular endothelial function under oxidative stress conditions [4]. These results are in line with a previous observation showing that activation of Nrf2 by Resveratrol-ameliorated oxidative stress and vascular calcification [45].…”

Section: Discussionsupporting

confidence: 93%

Hydrogen sulfide attenuates calcification of vascular smooth muscle cells via KEAP1/NRF2/NQO1 activation

et al. 2017

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Section: Discussionsupporting

confidence: 93%

Hydrogen sulfide attenuates calcification of vascular smooth muscle cells via KEAP1/NRF2/NQO1 activation

et al. 2017

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“…Data have shown that Res ameliorates inflammatory damage and protects against osteoarthritis in a rat model of osteoarthritis via NF‐κB and HO‐1/Nrf2 signaling . Res might protect rat vascular smooth muscle cells against redox injury induced by calcification through the involvement of the Nrf2 pathway . Once ROS exceed normal physiological limits, oxidative stress will be induced .…”

Section: Discussionmentioning

confidence: 99%

Nrf2–Keap1 pathway–mediated effects of resveratrol on oxidative stress and apoptosis in hydrogen peroxide–treated rheumatoid arthritis fibroblast‐like synoviocytes

Zhang

Wang

et al. 2019

Annals of the New York Academy of Sciences

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Resveratrol (Res) is a polyphenolic compound that has a variety of biological functions and activities. This study aimed to explore the mechanisms of the antioxidant and proapoptotic effects of Res in H2O2‐treated rheumatoid arthritis fibroblast‐like synoviocytes (RA‐FLSs) by the Nrf2–Keap1 signaling pathway. We found that 5 µM H2O2 promoted cell proliferation and increased intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) content in RA‐FLSs. However, Res could reverse these effects in 5 µMH2O2‐treated RA‐FLSs by (1) promoting expression of nuclear factor erythroid 2–related factor 2 (Nrf2) and heme oxygenase‐1 (HO‐1), (2) reducing expression of Kelch‐like ECH–related protein 1 (Keap1), (3) inhibiting production of ROS and MDA, (4) blocking activation of nuclear factor‐κB (NF‐κB) p65, (5) inhibiting cell proliferation and migration, and (6) activating Bcl‐2/Bax to induce apoptosis. After lentiviral silencing of Nrf2 (siNrf2) mRNA expression in RA‐FLSs, Res addition did not increase the expression of Nrf2 or HO‐1 to reduce the production of mitochondrial ROS caused by 5 µM H2O2. Res reduced the Bcl‐2/Bax ratio, but siNrf2 reduced the ability of Res to promote apoptosis. We conclude that Res inhibits ROS production by activating the Nrf2 pathway, thereby inhibiting activation of NF‐κB and proliferation and migration of RA‐FLSs, to induce apoptosis. Targeting the Nrf2–Keap1 pathway may be a relevant aim of using Res in the treatment of RA.

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“…By contrast, apurinic/apyrimidinic endonuclease 1/redox factor-1 (APE1/Ref-1), which plays a pleiotropic role in the reduction of ROS, was impaired during Pi-induced VSMC calcification [282]. Similarly, hydrogen peroxide and resveratrol were also effective in preventing VC, by augmentation of nuclear factor erythroid 2-related factor 2 (Nrf2) signaling [283,284]. resveratrol were also effective in preventing VC, by augmentation of nuclear factor erythroid 2related factor 2 (Nrf2) signaling [283,284].…”

Section: Mitochondrial Dysfunction and Defective Mitophagy In Vascumentioning

confidence: 99%

Vascular Calcification—New Insights into Its Mechanism

Lee

Jeon

2020

IJMS

258

254

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Vascular calcification (VC), which is categorized by intimal and medial calcification, depending on the site(s) involved within the vessel, is closely related to cardiovascular disease. Specifically, medial calcification is prevalent in certain medical situations, including chronic kidney disease and diabetes. The past few decades have seen extensive research into VC, revealing that the mechanism of VC is not merely a consequence of a high-phosphorous and -calcium milieu, but also occurs via delicate and well-organized biologic processes, including an imbalance between osteochondrogenic signaling and anticalcific events. In addition to traditionally established osteogenic signaling, dysfunctional calcium homeostasis is prerequisite in the development of VC. Moreover, loss of defensive mechanisms, by microorganelle dysfunction, including hyper-fragmented mitochondria, mitochondrial oxidative stress, defective autophagy or mitophagy, and endoplasmic reticulum (ER) stress, may all contribute to VC. To facilitate the understanding of vascular calcification, across any number of bioscientific disciplines, we provide this review of a detailed updated molecular mechanism of VC. This encompasses a vascular smooth muscle phenotypic of osteogenic differentiation, and multiple signaling pathways of VC induction, including the roles of inflammation and cellular microorganelle genesis.

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Resveratrol Ameliorated Vascular Calcification by Regulating Sirt-1 and Nrf2

Cited by 72 publications

References 29 publications

Hydrogen sulfide attenuates calcification of vascular smooth muscle cells via KEAP1/NRF2/NQO1 activation

Hydrogen sulfide attenuates calcification of vascular smooth muscle cells via KEAP1/NRF2/NQO1 activation

Nrf2–Keap1 pathway–mediated effects of resveratrol on oxidative stress and apoptosis in hydrogen peroxide–treated rheumatoid arthritis fibroblast‐like synoviocytes

Vascular Calcification—New Insights into Its Mechanism

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