ArticleJCI insight2019
TFEB activation in macrophages attenuates postmyocardial infarction ventricular dysfunction independently of ATG5-mediated autophagy.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 54 citations in OpenAlex.
- Sustained alternate-day fasting potentiates doxorubicin cardiotoxicity.Cell metabolism · 2023Trial
- Reprogramming macrophage metabolism for cardiovascular therapy: From molecular pathways to precision nanomedicine.Materials today. Bio · 2026Review
- TFEB Antagonizes Cardiac Hypertrophy and Failure by Enhancing Lysosomal Capacity and Mitochondrial Function.Circulation research · 2026Article
- Role of myeloid cell transcription factor EB in alcohol-induced liver injury in mice.Liver research (Beijing, China) · 2026Article
- Hotspots Evolution and Cutting-Edge Trends: A Bibliometric Analysis of Autophagy in Myocardial Infarction Studies From 2007 to 2025.Cardiovascular therapeutics · 2026Review
- Phosphorylation of CRYAB induces a condensatopathy to worsen post-myocardial infarction left ventricular remodeling.The Journal of clinical investigation · 2025Article
- Macrophage Polarization in Myocardial Ischemia‒Reperfusion Injury: Pathophysiology and Therapeutic Targets.Drug design, development and therapy · 2025Review
- Hypoxia sensing in resident cardiac macrophages regulates monocyte fate specification following ischemic heart injury.Nature cardiovascular research · 2024Article
- The Estrogen Receptor-Related Orphan Receptors Regulate Autophagy through TFEB.Molecular pharmacology · 2024Article
- Transcription Factor Activity Regulating Macrophage Heterogeneity during Skin Wound Healing.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Identification of mitophagy-related key genes and their correlation with immune cell infiltration in acute myocardial infarction via bioinformatics analysis.Frontiers in cardiovascular medicine · 2024Article
- Review
- Trehalose promotes atherosclerosis regression in female mice.Frontiers in cardiovascular medicine · 2024Article
- Crosstalk between myocardial autophagy and sterile inflammation in the development of heart failure.Autophagy reports · 2024Review
- Comprehensive view of macrophage autophagy and its application in cardiovascular diseases.Cell proliferation · 2024Review
- Cardiac radiation improves ventricular function in mice and humans with cardiomyopathy.Med (New York, N.Y.) · 2023Article
- Enhancing autophagy in CD11cCell reports · 2023Article
- Vps4a Regulates Autophagic Flux to Prevent Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2023Article
- The Role of Punicalagin and Its Metabolites in Atherosclerosis and Risk Factors Associated with the Disease.International journal of molecular sciences · 2023Review
- Apolipoprotein M Attenuates Anthracycline Cardiotoxicity and Lysosomal Injury.JACC. Basic to translational science · 2023Article
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 4 countries.
Funding
Abstract
Lysosomes are at the epicenter of cellular processes critical for inflammasome activation in macrophages. Inflammasome activation and IL-1β secretion are implicated in myocardial infarction (MI) and resultant heart failure; however, little is known about how macrophage lysosomes regulate these processes. In mice subjected to cardiac ischemia/reperfusion (IR) injury and humans with ischemic cardiomyopathy, we observed evidence of lysosomal impairment in macrophages. Inducible macrophage-specific overexpression of transcription factor EB (TFEB), a master regulator of lysosome biogenesis (Mϕ-TFEB), attenuated postinfarction remodeling, decreased abundance of proinflammatory macrophages, and reduced levels of myocardial IL-1β compared with controls. Surprisingly, neither inflammasome suppression nor Mϕ-TFEB-mediated attenuation of postinfarction myocardial dysfunction required intact ATG5-dependent macroautophagy (hereafter termed "autophagy"). RNA-seq of flow-sorted macrophages postinfarction revealed that Mϕ-TFEB upregulated key targets involved in lysosomal lipid metabolism. Specifically, inhibition of the TFEB target, lysosomal acid lipase, in vivo abrogated the beneficial effect of Mϕ-TFEB on postinfarction ventricular function. Thus, TFEB reprograms macrophage lysosomal lipid metabolism to attenuate remodeling after IR, suggesting an alternative paradigm whereby lysosome function affects inflammation.
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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.