Resveratrol protects cardiomyocytes against anoxia/reoxygenation via dephosphorylation of VDAC1 by Akt-GSK3 β pathway
Abstract
Our previous studies showed that the effect of resveratrol preventing mitochondrial permeability transition pore (mPTP) opening in myocardial ischemia/reperfusion injury was achieved by regulating voltage-dependent anion channel 1 (VDAC1). However, the underlying mechanism remains unclear. Previous studies demonstrated that the activity and function of VDAC1 are highly regulated by post-translational modification. In present study, we investigated whether resveratrol modulates VDAC1 phosphorylation to achieve cardioprotection and explored the signaling pathways involved. Our findings demonstrated that anoxia/reoxygenation (A/R) treatment, an ischemia/reperfusion model in vitro, enhanced VDAC1 phosphorylation in cardiomyocytes. Moreover, we found phosphorylated VDAC1 showed increased affinity to Bax, whereas interaction with hexokinase 2 (HK2) was reduced. Accordingly, the generation of reactive oxygen species increased, the mitochondrial membrane potential collapsed, mPTP opening increased and cytochrome c released into cytoplasm, thereby leading to increased apoptosis. Moreover, our data showed that pretreatment with resveratrol prior to A/R injury inhibited VDAC1 phosphorylation. Dephosphorylated VDAC1 using pretreated resveratrol promoted dissociation with Bax and binding to HK2, which subsequently protected cardiomyocytes against A/R injury. In addition, Akt and its downstream glycogen synthase kinase 3 β (GSK3β) were phosphorylated by the action of resveratrol. Akt inhibitor IV abrogated Akt-GSK3β phosphorylation and thereby abolished the dephosphorylation activity of resveratrol on VDAC1. Moreover, all resveratrol-mediated protective effects on A/R injured cardiomyocytes were abolished by Akt inhibitor IV. Taken together, our data indicated that A/R injury enhanced VDAC1 phosphorylation in cardiomyocytes, whereas pretreatment with resveratrol dephosphorylated VDAC1 through the Akt-GSK3β pathway, thereby protecting cardiomyocytes against A/R injury.
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The effect of resveratrol on autophagy and mitophagy depends on inhibition of mPTP.
“and it appears that this effect also depends on the inhibition of mPTP [265,266,267,268].”
From The mitochondrial permeability transition: Nexus of aging, disease and longevity (2021) · cites this paper as [268]
Resveratrol protects against I/R damage in myocytes by dephosphorylation of VDAC1, which inhibits mPTP.
“Resveratrol protects against I/R damage in myocytes by the dephosphorylation of VDAC1, which inhibits mPTP [268].”
From The mitochondrial permeability transition: Nexus of aging, disease and longevity (2021) · cites this paper as [268]
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- Authors
- Tian, M., Xie, Y., Meng, Y., Ma, W., Tong, Z., Yang, X., Lai, S., Zhou, Y., He, M., & Liao, Z.
- Affiliations
- Nanchang University (CN)
- Jiangxi University of Traditional Chinese Medicine (CN)
- First Affiliated Hospital of Nanchang University (CN)
- Corresponding author
- Liao, Zhangping
- Venue
- European Journal of Pharmacology
- Publisher
- Elsevier BV
- Published
- 2019-01
- Volume
- 843
- Pages
- 80-87
- ISSN
- 0014-2999 (ISSN-L)
- OpenAlex
- W2901649628
- Cited by
- 53
- References
- 44
- Citations by year
- 2026: 5 · 2025: 8 · 2024: 6 · 2023: 4 · 2022: 4 · 2021: 9 · 2020: 9 · 2019: 8
- FWCI
- 4.94
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- European Journal of Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81460495, 81660601)
- Natural Science Foundation of Jiangxi Province (20142BAB215016)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- resveratrol, cardioprotection, anoxia/reoxygenation injury, cardiomyocytes, VDAC1, dephosphorylation, Akt/GSK-3β signaling, mitochondrial permeability transition pore, Bax, hexokinase 2, reactive oxygen species, mitochondrial membrane potential, cytochrome c release, apoptosis, myocardial ischemia-reperfusion injury
- MeSH terms
- Glycogen Synthase Kinase 3 beta, Resveratrol, Animals, Animals, Newborn, Cardiotonic Agents, Cells, Cultured, Phosphorylation, Cell Hypoxia, Rats, Sprague-Dawley, Apoptosis, Myocytes, Cardiac, Voltage-Dependent Anion Channel 1, Proto-Oncogene Proteins c-akt
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