ArticleInflammation2023
LPS-aggravated Ferroptosis via Disrupting Circadian Rhythm by Bmal1/AKT/p53 in Sepsis-Induced Myocardial Injury.
Article in Inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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
21 citing papers in PubMed, 25 citations in OpenAlex.
- Ferroptosis as a target mechanism in heart and kidney disease.The Journal of clinical investigation · 2026Review
- Beyond the Pump: Unravelling Immunometabolic Crosstalk and Organelle Dynamics in Sepsis-Induced Cardiomyopathy.Journal of cardiovascular translational research · 2026Article
- The Interactions Between Circadian Rhythm, Gut Microbiota, and Anxiety: From Mechanisms to Intervention Strategies.Nutrients · 2026Review
- Role of oxidative stress in sepsis: Mechanisms, pathways, and therapeutic strategies.Journal of pharmaceutical analysis · 2026Review
- The interplay between circadian rhythm components and apoptosis in health and disease.Human cell · 2026Review
- Molecular subtyping and immune microenvironment heterogeneity in pediatric influenza-associated prolonged multiple organ dysfunction syndrome.Translational pediatrics · 2026Article
- Melatonin-engineered MSCs-exosomes deliver USP4 to stabilise ARNTL and inhibit clock rhythmic ferroptosis for enhanced flap survival.Clinical and translational medicine · 2026Article
- Targeting ferroptosis in sepsis-induced cardiomyopathy: mechanisms and therapeutic potential of traditional Chinese Medicine.Frontiers in pharmacology · 2026Review
- Ferroptosis in Cardiovascular Diseases and Ferroptosis-Related Intervention Approaches.Cardiovascular drugs and therapy · 2025Review
- Precision Profiling of Disease Progression in Murine Models of Sepsis and Septic Shock.International journal of molecular sciences · 2025Article
- New developments in the role of ferroptosis in sepsis‑induced cardiomyopathy (Review).Molecular medicine reports · 2025Review
- Integrating bioinformatics and machine learning to discover sumoylation associated signatures in sepsis.Scientific reports · 2025Article
- Estrogen replacement restores period 2-mediated inhibition of ferroptosis and mitigates cardiac dysfunction in estrogen-deficient rats.The Journal of pharmacology and experimental therapeutics · 2025Article
- The role of programmed cell death in organ dysfunction induced by opportunistic pathogens.Critical care (London, England) · 2025Review
- Basic helix-loop-helix ARNT like 1 regulates the function of immune cells and participates in the development of immune-related diseases.Burns & trauma · 2025Review
- Unveiling the novel role of circadian rhythms in sepsis and septic shock: unexplored implications for chronotherapy.Frontiers in endocrinology · 2025Review
- Time of day-dependent alterations of ferroptosis in LPS-induced myocardial injury via Bmal-1/AKT/ Nrf2 in rat and H9c2 cell.Heliyon · 2024Article
- Insights from bioinformatics analysis reveal that lipopolysaccharide induces activation of chemokine-related signaling pathways in human nasal epithelial cells.Scientific reports · 2024Article
- Deciphering ferroptosis in critical care: mechanisms, consequences, and therapeutic opportunities.Frontiers in immunology · 2024Review
- Ferroptosisand Its Role in the Treatment of Sepsis-Related Organ Injury: Mechanisms and Potential Therapeutic Approaches.Infection and drug resistance · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Circadian disruption is involved in the progress of sepsis-induced cardiomyopathy (SICM), one of the leading causes of death in sepsis. The molecular mechanism remains ambiguous. In this study, LPS was used to build SICM model in H9c2 cell. The results suggested that LPS induced cytotoxicity via increasing ferroptosis over the time of course. After screening the expressions of six circadian genes, the circadian swing of Bmal1 was dramatically restrained by LPS in H9c2 cell of SIMC vitro model. PcDNA and siRNA were used to upregulate and downregulate Bmal1 and confirmed that Bmal1 inhibited LPS-triggered ferroptosis in H9c2 cells. Then, the results suggested that AKT/p53 pathway was restrained by LPS in H9c2 cell. Rescue test indicated that Bmal1 inhibited LPS-triggered ferroptosis via AKT/p53 pathway in H9c2 cells. In summary, our findings demonstrated that LPS induced cytotoxicity via increasing ferroptosis over the time of course in H9c2 cells and Bmal1 inhibited this toxicity of LPS via AKT/p53 pathway. Although further studies are needed, our findings may contribute to a new insight to mechanism of SICM.
Indexed as
Identifiers
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.