ArticleEMBO molecular medicine2019
3,4-Dimethoxychalcone induces autophagy through activation of the transcription factors TFE3 and TFEB.
Article in EMBO molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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Who cites it
41 citing papers in PubMed, 62 citations in OpenAlex.
- 3,4-Dimethoxychalcone-induced caloric restriction inhibits PANoptosis to promote ischemic and diabetic skin flap survival: experimental studies.International journal of surgery (London, England) · 2026Article
- The geroprotective potential of chalcones.Nature communications · 2025Review
- Anti-ageing interventions for the treatment of cardiovascular disease.Cardiovascular research · 2025Review
- Lysosomes as Dynamic Regulators of Metabolic Signaling and Organ Physiology in Aging: From Mechanism to Therapy.Aging and disease · 2025Review
- Impact of psychological stress on ovarian function: Insights, mechanisms and intervention strategies (Review).International journal of molecular medicine · 2025Review
- Oligodendroglial fatty acid metabolism as a central nervous system energy reserve.Nature neuroscience · 2024Article
- Sex differences in response to obesity and caloric restriction on cognition and hippocampal measures of autophagic-lysosomal transcripts and signaling pathways.BMC neuroscience · 2024Article
- Benzodiazepines compromise the outcome of cancer immunotherapy.Oncoimmunology · 2024Article
- 3,4-dimethoxychalcone induces autophagy and reduces neointimal hyperplasia and aortic lesions in mouse models of atherosclerosis.Cell death & disease · 2023Article
- Adipose tissue macrophages: implications for obesity-associated cancer.Military Medical Research · 2023Review
- Autophagy and neurodegeneration: Unraveling the role of C9ORF72 in the regulation of autophagy and its relationship to ALS-FTD pathology.Frontiers in cellular neuroscience · 2023Review
- 3,4-Dimethoxychalcone, a caloric restriction mimetic, enhances TFEB-mediated autophagy and alleviates pyroptosis and necroptosis after spinal cord injury.Theranostics · 2023Article
- Review
- Dietary regulation in health and disease.Signal transduction and targeted therapy · 2022Review
- Pharmacophore optimization of imidazole chalcones to modulate microtubule dynamics.Bioorganic chemistry · 2022Article
- The role of autophagy in death of cardiomyocytes.Journal of molecular and cellular cardiology · 2022Review
- Anthelmintics nitazoxanide protects against experimental hyperlipidemia and hepatic steatosis in hamsters and mice.Acta pharmaceutica Sinica. B · 2022Article
- Article
- Autophagy activation by dietary piceatannol enhances the efficacy of immunogenic chemotherapy.Frontiers in immunology · 2022Article
- Targeting lysosomes in human disease: from basic research to clinical applications.Signal transduction and targeted therapy · 2021Review
Corrections and comments
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Authors and funding
21 authors at 6 institutions in 7 countries.
Funding
Abstract
Caloric restriction mimetics (CRMs) are natural or synthetic compounds that mimic the health-promoting and longevity-extending effects of caloric restriction. CRMs provoke the deacetylation of cellular proteins coupled to an increase in autophagic flux in the absence of toxicity. Here, we report the identification of a novel candidate CRM, namely 3,4-dimethoxychalcone (3,4-DC), among a library of polyphenols. When added to several different human cell lines, 3,4-DC induced the deacetylation of cytoplasmic proteins and stimulated autophagic flux. At difference with other well-characterized CRMs, 3,4-DC, however, required transcription factor EB (TFEB)- and E3 (TFE3)-dependent gene transcription and mRNA translation to trigger autophagy. 3,4-DC stimulated the translocation of TFEB and TFE3 into nuclei both in vitro and in vivo, in hepatocytes and cardiomyocytes. 3,4-DC induced autophagy in vitro and in mouse organs, mediated autophagy-dependent cardioprotective effects, and improved the efficacy of anticancer chemotherapy in vivo. Altogether, our results suggest that 3,4-DC is a novel CRM with a previously unrecognized mode of action.
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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.