ArticleAging2021
FAM134B-mediated endoplasmic reticulum autophagy protects against sepsis myocardial injury in mice.
Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- The emerging role of ERphagy/reticulophagy in pathogen invasion.Autophagy · 2026Article
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- ER-phagy receptors: structural mechanisms in selective ER degradation and disease implications.Acta pharmacologica Sinica · 2026Review
- The immune regulation and signaling transduction of FAM134B-mediated endoplasmic reticulum-phagy in ferroptosis of dendritic cells after sepsis.Journal of advanced research · 2026Article
- Nur77 attenuates Paneth cell necroptosis-induced intestinal inflammation through regulating endoplasmic reticulum homeostasis in sepsis.Journal of advanced research · 2026Article
- Endoplasmic reticulum autophagy in inflammatory diseases.Frontiers in immunology · 2026Review
- Article
- Engineered endoplasmic reticulum-targeting nanodrugs with Piezo1 inhibition and promotion of cell uptake for subarachnoid hemorrhage inflammation repair.Journal of nanobiotechnology · 2025Article
- Research Hotspots and Frontier Trends of Autophagy in Diabetic Cardiomyopathy From 2014 to 2024: A Bibliometric Analysis.Journal of multidisciplinary healthcare · 2025Article
- Nuclear fragile X mental retardation-interacting protein 1-mediated ribophagy regulates immune function of dendritic cells in polymicrobial sepsis.Burns & trauma · 2025Article
- FAM134B in Cellular Homeostasis: Bridging Endoplasmic Reticulum-Phagy to Human Diseases.International journal of biological sciences · 2025Review
- Dexmedetomidine ameliorates x-ray-induced myocardial injury via alleviating cardiomyocyte apoptosis and autophagy.BMC cardiovascular disorders · 2024Article
- Qingre Huoxue decoction attenuates myocardial ischemia‒reperfusion injury by regulating the autophagy‒endoplasmic reticulum stress axis via FAM134B-mediated ER-phagy.Frontiers in pharmacology · 2024Article
- Matrine Alleviates Sepsis-Induced Myocardial Injury by Inhibiting Ferroptosis and Apoptosis.Inflammation · 2023Article
- [Influence of family with sequence similarity 134, member B-mediated reticulophagy on lipopolysaccharide-induced apoptosis of mouse dendritic cells].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2023Article
- Role of endoplasmic reticulum autophagy in acute lung injury.Frontiers in immunology · 2023Review
- Protective effect and mechanism of γ-secretase inhibitor on myocardial injury in sepsis rats.American journal of translational research · 2023Article
- A novel interleukin-2-based fusion molecule, HCW9302, differentially promotes regulatory T cell expansion to treat atherosclerosis in mice.Frontiers in immunology · 2023Article
- MiR-501-5p alleviates cardiac dysfunction in septic patients through targeting NR4A3 to prevent its binding with Bcl-2.Cell cycle (Georgetown, Tex.) · 2022Article
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reticulophagy regulator 1 (RETEG1, also known as FAM134B) plays a crucial role in endoplasmic reticulum autophagy. We aimed to explore the effect of FAM134B-mediated endoplasmic reticulum autophagy in sepsis myocardial injury in mice. Sepsis myocardial injury mice were established via cecal ligation and puncture procedures. The expression of FAM134B and LC3-II/I was determined using immunohistochemistry. Myocardial tissue morphological changes and apoptosis were examined using hematoxylin and eosin (H&E) staining and TUNEL analysis. The effects of FAM134B knockdown or overexpression on mice with sepsis myocardial injury were also studied. The levels of TNF-α, IL-6, IL-8, and IL-10 were evaluated using enzyme-linked immunosorbent assay (ELISA). Autophagy- and apoptosis-related protein expression was detected using western blotting. The effect of FAM134B on Lipopolysaccharide (LPS) -induced cardiomyocytes was also studied. The expression of FAM134B and LC3-II/I increased in sepsis mice and lipopolysaccharide (LPS)-treated cardiomyocytes. 3-Methyladenine (3-MA) significantly inhibited FAM134B and LC3-II/I expression and promoted myocardial injury, inflammation response, and cardiomyocyte apoptosis. The overexpression of FAM134B could minimize myocardial injury, inflammation, and apoptosis, whereas FAM134B knockdown showed opposite effects. FAM134B-mediated endoplasmic reticulum autophagy had a protective effect on sepsis myocardial injury in mice by reducing inflammation and tissue apoptosis, which may provide new insights for sepsis myocardial injury therapies.
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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.