ReviewJournal of intensive care2024
Autophagy and autophagic cell death in sepsis: friend or foe?
Review in Journal of intensive care, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Research trends and topics on sepsis immunosuppression: a bibliometric and visual analysis of global research from 2004 to 2024.Frontiers in medicine · 2025Pooled it
- Article
- Organelle Crosstalk and Metabolic Reprogramming in Idiopathic Pulmonary Fibrosis: Mechanisms and Therapeutic Implications.Cell biochemistry and function · 2026Review
- PINK1-Parkin pathway-mediated mitophagy in sepsis: friend or foe?Molecular biology reports · 2026Review
- The role of cellular senescence in sepsis and its mechanism in copper death: An analysis based on machine learning.Medicine · 2026Article
- Low-dose esmolol attenuates sepsis-induced myocardial injury: association with improved autophagic homeostasis and PI3K/Akt signaling.Journal of intensive care · 2026Article
- Article
- Targeting FoxO1/3a, NF-κB, and mTOR signaling attenuates muscle atrophy in sepsis.Scientific reports · 2026Article
- ATG5 overexpression enhances the therapeutic efficacy of mesenchymal stem cells in a mouse colitis model by augmenting anti-inflammatory and antioxidative mechanisms.Stem cell research & therapy · 2026Article
- LCN2 aggravates sepsis-induced ALI by inhibiting MUC1 to activate ER-stress-autophagy induced ferroptosis via lactate/MCT1/AMPK/mTOR axis.Apoptosis : an international journal on programmed cell death · 2026Article
- Modulating Vimentin: A Systems-Level Therapeutic Strategy for Sepsis and Complex Diseases.Life (Basel, Switzerland) · 2026Article
- Autophagy-ferroptosis crosstalk in sepsis: metabolic pathways, redox injury, and host-directed antioxidant nanomedicine.Frontiers in immunology · 2026Review
- miR-1248 enhances bortezomib-induced autophagy by targeting MEF2C/p38-MAPK signaling in multiple myeloma.Frontiers in oncology · 2026Article
- PCSK9 inhibition alleviates sepsis-induced myocardial dysfunction by facilitating PINK1/parkin-associated mitophagy.Frontiers in pharmacology · 2026Article
- Aryl hydrocarbon receptor regulates programmed cell death in diseases: molecular mechanisms and therapeutic implications.Frontiers in immunology · 2026Review
- Modulation of mitochondrial quality control in sepsis by traditional Chinese medicine: mechanistic insights and translational perspectives.Frontiers in pharmacology · 2026Review
- Crosstalk between innate immune signaling pathways and integrated TLR, NLRP3 inflammasome, cGAS-STING, and NF-κB networks in sepsis.Frontiers in cell and developmental biology · 2026Review
- Source-stratified gut-extraintestinal organ crosstalk in sepsis-associated acute gastrointestinal injury and paralytic ileus: the gut as both driver and target.Frontiers in medicine · 2026Review
- Controversial effects of metformin on human physiology and pathophysiology.Frontiers in pharmacology · 2026Review
- Unveiling the neuroprotective power: the role of autophagy in remote ischemic conditioning.Metabolic brain disease · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In sepsis, inflammation, and nutrient deficiencies endanger cellular homeostasis and survival. Autophagy is primarily a mechanism of cellular survival under fasting conditions. However, autophagy-dependent cell death, known as autophagic cell death, is proinflammatory and can exacerbate sepsis. Autophagy also regulates various types of non-inflammatory and inflammatory cell deaths. Non-inflammatory apoptosis tends to suppress inflammation, however, inflammatory necroptosis, pyroptosis, ferroptosis, and autophagic cell death lead to the release of inflammatory cytokines and damage-associated molecular patterns (DAMPs) and amplify inflammation. The selection of cell death mechanisms is complex and often involves a mixture of various styles. Similarly, protective autophagy and lethal autophagy may be triggered simultaneously in cells. How cells balance the regulatory mechanisms of these processes is an area of interest that is still under investigation. Therapies aimed at modulating autophagy are considered promising. Enhancing autophagy helps clear and recycle damaged organelles and reduce the burden of inflammatory processes while inhibiting excessive autophagy, which could prevent autophagic cell death. In this review, we introduce recent advances in research and the complex regulatory system of autophagy in sepsis.
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What Socratic holds
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 Socratic graph.