ArticleMolecular neurobiology2017
Reduction in Autophagy by (-)-Epigallocatechin-3-Gallate (EGCG): a Potential Mechanism of Prevention of Mitochondrial Dysfunction After Subarachnoid Hemorrhage.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 49 citations in OpenAlex.
- Catechins in stroke: multi-target mechanisms, preclinical evidence, and translational challenges.Frontiers in pharmacology · 2026Review
- Ferroptosis and Metabolic Dysregulation: Emerging Chemical Targets in Cancer and Infection.Molecules (Basel, Switzerland) · 2025Review
- Polyphenols in the Central Nervous System: Cellular Effects and Liposomal Delivery Approaches.International journal of molecular sciences · 2025Review
- Epigallocatechin 3-gallate-induced neuroprotection in neurodegenerative diseases: molecular mechanisms and clinical insights.Molecular and cellular biochemistry · 2025Review
- Harvesting Health: Phytochemicals in Cognitive Impairment Therapy.Central nervous system agents in medicinal chemistry · 2025Review
- Microneedles: A Versatile Drug Delivery Carrier for Phytobioactive Compounds as a Therapeutic Modulator for Targeting Mitochondrial Dysfunction in the Management of Neurodegenerative Diseases.Current neuropharmacology · 2024Review
- The blood-brain barrier and the neurovascular unit in subarachnoid hemorrhage: molecular events and potential treatments.Fluids and barriers of the CNS · 2022Review
- ACE2 Rescues Impaired Autophagic Flux Through the PI3K/AKT Pathway After Subarachnoid Hemorrhage.Neurochemical research · 2022Article
- New Mechanisms and Targets of Subarachnoid Hemorrhage: A Focus on Mitochondria.Current neuropharmacology · 2022Review
- Evaluation of the synergistic effects of epigallocatechin-3-gallate-loaded PEGylated-PLGA nanoparticles with nimodipine against neuronal injury after subarachnoid hemorrhage.Frontiers in nutrition · 2022Article
- Mitochondrial dysfunction associated with autophagy and mitophagy in cerebrospinal fluid cells of patients with delayed cerebral ischemia following subarachnoid hemorrhage.Scientific reports · 2021Article
- Neuroprotective Strategies in Aneurysmal Subarachnoid Hemorrhage (aSAH).International journal of molecular sciences · 2021Review
- Natural products targeting mitochondria: emerging therapeutics for age-associated neurological disorders.Pharmacology & therapeutics · 2021Review
- EGCG Promotes Neurite Outgrowth through the IntegrinEvidence-based complementary and alternative medicine : eCAM · 2021Article
- From Preclinical Stroke Models to Humans: Polyphenols in the Prevention and Treatment of Stroke.Nutrients · 2020Review
- The Role of Epigallocatechin-3-Gallate in Autophagy and Endoplasmic Reticulum Stress (ERS)-Induced Apoptosis of Human Diseases.Medical science monitor : international medical journal of experimental and clinical research · 2020Review
- Neuroprotective Properties of Green Tea (Molecules (Basel, Switzerland) · 2020Review
- Review
- Receptor-Mediated Delivery of Astaxanthin-Loaded Nanoparticles to Neurons: An Enhanced Potential for Subarachnoid Hemorrhage Treatment.Frontiers in neuroscience · 2019Article
- Neuroprotective Role of Phytochemicals.Molecules (Basel, Switzerland) · 2018Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction and subsequent autophagy, which are common features in central nervous system (CNS) disorders, were found to contribute to neuronal cell injury after subarachnoid hemorrhage (SAH). (-)-Epigallocatechin-3-gallate (EGCG), the main biological active of tea catechin, is well known for its beneficial effects in the treatment of CNS diseases. Here, the ability of EGCG to rescue cellular injury and mitochondrial function following the improvement of autophagic flux after SAH was investigated. As expected, EGCG-protected mitochondrial function depended on the inhibition of cytosolic Ca
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.