ArticleScientific reports2016
Mitochondria-targeted esculetin alleviates mitochondrial dysfunction by AMPK-mediated nitric oxide and SIRT3 regulation in endothelial cells: potential implications in atherosclerosis.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 59 citations in OpenAlex.
- Natural Small Molecules Targeting Mitochondrial Quality Control for the Treatment of Metabolic Diseases: Mechanisms, Novel Formulations, and Translational Perspectives.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Plasma exosome-derived miRNA-887-5p alleviates high glucose- and lipid-induced endothelial cell dysfunction.Nutrition & diabetes · 2026Article
- Mitochondrial dysfunction in endothelial senescence: implications for vascular remodeling and therapeutic strategies.Archives of pharmacal research · 2026Review
- How to measure and model cardiovascular aging.Cardiovascular research · 2025Review
- Review
- Centenarians-the way to healthy vascular ageing and longevity: a review from VascAgeNet.GeroScience · 2025Review
- Role of AMPK and Sirtuins in Aging Heart: Basic and Translational Aspects.Aging and disease · 2024Review
- Mitochondrial quality control in human health and disease.Military Medical Research · 2024Review
- Therapeutic efficacies of mitochondria-targeted esculetin and metformin in the improvement of age-associated atherosclerosis via regulating AMPK activation.GeroScience · 2024Article
- The Coumarin-Derivative Esculetin Protects against Lipotoxicity in Primary Rat Hepatocytes via Attenuating JNK-Mediated Oxidative Stress and Attenuates Free Fatty Acid-Induced Lipid Accumulation.Antioxidants (Basel, Switzerland) · 2023Article
- Esculetin Alleviates Inflammation, Oxidative Stress and Apoptosis in Intestinal Ischemia/Reperfusion Injury via Targeting SIRT3/AMPK/mTOR Signaling and Regulating Autophagy.Journal of inflammation research · 2023Article
- SIRT3 attenuates coronary atherosclerosis in diabetic patients by regulating endothelial cell function.Journal of clinical laboratory analysis · 2022Article
- Mitochondria Related Cell Death Modalities and Disease.Frontiers in cell and developmental biology · 2022Review
- Naringenin ameliorates homocysteine induced endothelial damage via the AMPKα/Sirt1 pathway.Journal of advanced research · 2021Article
- Idebenone Protects against Atherosclerosis in Apolipoprotein E-Deficient Mice Via Activation of the SIRT3-SOD2-mtROS Pathway.Cardiovascular drugs and therapy · 2021Article
- Heme Oxygenase-1 at the Nexus of Endothelial Cell Fate Decision Under Oxidative Stress.Frontiers in cell and developmental biology · 2021Article
- Novel Insights and Current Evidence for Mechanisms of Atherosclerosis: Mitochondrial Dynamics as a Potential Therapeutic Target.Frontiers in cell and developmental biology · 2021Review
- Butyrate mitigates TNF-α-induced attachment of monocytes to endothelial cells.Journal of bioenergetics and biomembranes · 2020Article
- AMPK, Mitochondrial Function, and Cardiovascular Disease.International journal of molecular sciences · 2020Review
- NADPH oxidases and oxidase crosstalk in cardiovascular diseases: novel therapeutic targets.Nature reviews. Cardiology · 2020Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria-targeted compounds are emerging as a new class of drugs that can potentially alter the pathophysiology of those diseases where mitochondrial dysfunction plays a critical role. We have synthesized a novel mitochondria-targeted esculetin (Mito-Esc) with an aim to investigate its effect during oxidative stress-induced endothelial cell death and angiotensin (Ang)-II-induced atherosclerosis in ApoE(-/-) mice. Mito-Esc but not natural esculetin treatment significantly inhibited H2O2- and Ang-II-induced cell death in human aortic endothelial cells by enhancing NO production via AMPK-mediated eNOS phosphorylation. While L-NAME (NOS inhibitor) significantly abrogated Mito-Esc-mediated protective effects, Compound c (inhibitor of AMPK) significantly decreased Mito-Esc-mediated increase in NO production. Notably, Mito-Esc promoted mitochondrial biogenesis by enhancing SIRT3 expression through AMPK activation; and restored H2O2-induced inhibition of mitochondrial respiration. siSIRT3 treatment not only completely reversed Mito-Esc-mediated mitochondrial biogenetic marker expressions but also caused endothelial cell death. Furthermore, Mito-Esc administration to ApoE(-/-) mice greatly alleviated Ang-II-induced atheromatous plaque formation, monocyte infiltration and serum pro-inflammatory cytokines levels. We conclude that Mito-Esc is preferentially taken up by the mitochondria and preserves endothelial cell survival during oxidative stress by modulating NO generation via AMPK. Also, Mito-Esc-induced SIRT3 plays a pivotal role in mediating mitochondrial biogenesis and perhaps contributes to its anti-atherogenic effects.
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