ArticleOxidative medicine and cellular longevity2018
Epigallocatechin-3-Gallate (EGCG) Promotes Autophagy-Dependent Survival via Influencing the Balance of mTOR-AMPK Pathways upon Endoplasmic Reticulum Stress.
Article in Oxidative medicine and cellular longevity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.
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Who cites it
64 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.
- Nutraceutical Approaches of Autophagy and Neuroinflammation in Alzheimer's Disease: A Systematic Review.Molecules (Basel, Switzerland) · 2020Pooled it
- EGCG targeting autophagy in cardiovascular diseases: mechanisms and therapeutic potential.Molecular biology reports · 2026Review
- Heavy metal toxicity as a driver of endoplasmic reticulum stress and dysfunction.The FEBS journal · 2026Review
- Natural modulators of enhancer of zeste homolog 2 (EZH2): potential epigenetic regulators of aging-associated pathways.Biogerontology · 2026Review
- Chemical and Molecular Strategies in Restoring Autophagic Flux in TDP-43 Proteinopathy.Molecules (Basel, Switzerland) · 2026Review
- Mechanistic Modulation of Autophagy by Bioactive Natural Products: Implications for Human Aging and Longevity.Nutrients · 2026Review
- Bioactive Phytochemicals in Experimental Models of Multiple Sclerosis: Mechanisms, Efficacy, and Translational Potential.Nutrients · 2026Review
- Plant polyphenols as context-dependent modulators of cellular signalling networks.Frontiers in nutrition · 2026Review
- Cell-specific roles of autophagy in liver fibrosis: implications for targeted pharmacotherapy.Annals of medicine · 2025Review
- Fine-Tuning of the Endoplasmic Reticulum Stress Response Mechanism Plays a Key Role in Cellular Survival-A Mathematical Study.International journal of molecular sciences · 2025Article
- The Supportive Role of Plant-Based Substances in AMD Treatment and Their Potential.International journal of molecular sciences · 2025Review
- The Fundamental Role of Nutrients for Metabolic Balance and Epigenome Integrity Maintenance.Epigenomes · 2025Review
- Green Tea Mitigates the Hallmarks of Aging and Age-Related Multisystem Deterioration.Aging and disease · 2025Review
- Enhancing the bioavailability and activity of natural antioxidants with nanobubbles and nanoparticles.Redox report : communications in free radical research · 2024Review
- Review
- Immunomodulatory Effects of Green Tea Catechins and Their Ring Fission Metabolites in a Tumor Microenvironment Perspective.Molecules (Basel, Switzerland) · 2024Review
- Epigallocatechin-3-gallate protects bovine ruminal epithelial cells against lipopolysaccharide-induced inflammatory damage by activating autophagy.Journal of animal science and biotechnology · 2024Article
- Mechanism of Decision Making between Autophagy and Apoptosis Induction upon Endoplasmic Reticulum Stress.International journal of molecular sciences · 2024Review
- Natural Phenolic Compounds with Neuroprotective Effects.Neurochemical research · 2024Review
- Epigallocatechin-3-Gallate and Genistein for Decreasing Gut Dysbiosis, Inhibiting Inflammasomes, and Aiding Autophagy in Alzheimer's Disease.Brain sciences · 2024Review
4 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The maintenance of cellular homeostasis is largely dependent on the ability of cells to give an adequate response to various internal and external stimuli. We have recently proposed that the life-and-death decision in endoplasmic reticulum (ER) stress response is defined by a crosstalk between autophagy, apoptosis, and mTOR-AMPK pathways, where the transient switch from autophagy-dependent survival to apoptotic cell death is controlled by GADD34. The aim of the present study was to investigate the role of epigallocatechin-3-gallate (EGCG), the major polyphenol of green tea, in promoting autophagy-dependent survival and to verify the key role in connecting GADD34 with mTOR-AMPK pathways upon prolonged ER stress. Our findings, obtained by using HEK293T cells, revealed that EGCG treatment is able to extend cell viability by inducing autophagy. We confirmed that EGCG-induced autophagy is mTOR-dependent and PKA-independent; furthermore, it also required ULK1. We show that pretreatment of cells with EGCG diminishes the negative effect of GADD34 inhibition (by guanabenz or siGADD34 treatment) on autophagy. EGCG was able to delay apoptotic cell death by upregulating autophagy-dependent survival even in the absence of GADD34. Our data suggest a novel role for EGCG in promoting cell survival via shifting the balance of mTOR-AMPK pathways in ER stress.
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