ReviewCell stress2017
Emerging roles of mitochondria and autophagy in liver injury during sepsis.
Review in Cell stress, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- Sepsis and the Liver.Diseases (Basel, Switzerland) · 2025Review
- Protective effects of chlorogenic acid on hepatic injury in piglets challenged with lipopolysaccharide: a preliminary study.Veterinary research communications · 2025Article
- Time-Resolved Metabolomics Reveals Mitochondrial Protection in Septic Liver Injury.Metabolites · 2025Article
- Pyrrolidine Dithiocarbamate Ameliorates Sepsis-Associated Encephalopathy by Inhibiting Autophagy and Inflammation in the Brain.Neurochemical research · 2025Article
- Association of Autophagy-Related Gene 5 (ATG5) With Neonatal Cholestasis in Egyptian Pediatric Patients.Iranian journal of pathology · 2025Article
- Autophagy and autophagic cell death in sepsis: friend or foe?Journal of intensive care · 2024Review
- Starvation Protects Hepatocytes from Inflammatory Damage through Paradoxical mTORC1 Signaling.Cells · 2023Article
- Redox Activation of Mitochondrial DAMPs and the Metabolic Consequences for Development of Autoimmunity.Antioxidants & redox signaling · 2022Review
- Metabolome Characteristics of Liver Autophagy Deficiency under Starvation Conditions in Infancy.Nutrients · 2021Article
- The role and mechanism of PKM2 in the development of LPS-induced acute kidney injury.Histology and histopathology · 2021Article
- Autophagy in liver diseases.World journal of hepatology · 2021Review
- Article
- CpG-Oligodeoxynucleotides Alleviate Tert-Butyl Hydroperoxide-Induced Macrophage Apoptosis by Regulating Mitochondrial Function and Suppressing ROS Production.Oxidative medicine and cellular longevity · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent research indicates crucial roles of autophagy during sepsis. In animal models of sepsis induced by cecal ligation and puncture (CLP) or the systemic administration of lipopolysaccharides (LPS), autophagy is implicated in the activation and/or damage of various cells/organs, such as immune cells, heart, lung, kidney, and liver. Since sepsis is associated with an increased production of pro- as well as anti-inflammatory cytokines, it has long been considered that hypercytokinemia is a fetal immune response leading to multiple organ failure (MOF) and mortality of humans during sepsis. However, a recent paradigm illuminates the crucial roles of mitochondrial dysfunction as well as the perturbation of autophagy in the pathogenesis of sepsis. In the livers of animal models of sepsis, autophagy is involved in the elimination of damaged mitochondria to prevent the generation of mitochondrial ROS and the initiation of the mitochondrial apoptotic pathway. In addition, many reports now indicate that the role of autophagy is not restricted to the elimination of hazardous malfunctioning mitochondria within the cells; autophagy has been shown to be involved in the regulation of inflammasome activation and the release of cytokines as well as other inflammatory substances. In this review, we summarize recent literature describing the versatile role of autophagy and its possible implications in the pathogenesis of sepsis in the liver.
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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.