ArticleCell death discovery2022
ICA69 aggravates ferroptosis causing septic cardiac dysfunction via STING trafficking.
Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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.
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.
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Who cites it
40 citing papers in PubMed, 61 citations in OpenAlex.
- Ferroptosis as a target mechanism in heart and kidney disease.The Journal of clinical investigation · 2026Review
- The emerging Nexus of STING signaling and ferroptosis: from mechanisms to therapeutic opportunities.Cell death discovery · 2026Review
- Targeting ferroptosis in sepsis-induced cardiomyopathy: mechanisms and therapeutic potential of traditional Chinese Medicine.Frontiers in pharmacology · 2026Review
- Bridging innate immunity and iron-dependent death: the interplay between cyclic GMP-AMP synthase-stimulator of interferon genes nexus and ferroptosis in cancer and inflammation.Frontiers in cell and developmental biology · 2026Review
- (+)-JQ1 Upregulates SIRT3 to Suppress cGAS/STING Pathway-Mediated Neuronal Inflammation and Ferroptosis After Hypoxic-Ischemic Encephalopathy.Drug design, development and therapy · 2026Article
- Interplay of cGAS-STING and ferroptosis: crosstalk, molecular mechanisms, and therapeutic prospects.Archives of toxicology · 2025Review
- The emerging role of ferroptosis in the pathological development and progression of sepsis.Military Medical Research · 2025Review
- Targeting Lcn2 to Inhibit Myocardial Cell Ferroptosis is a Potential Therapy for Alleviating Septic Cardiomyopathy.Inflammation · 2025Article
- Cardiomyocyte mitochondrial mono-ADP-ribosylation dictates cardiac tolerance to sepsis by configuring bioenergetic reserve in male mice.Nature communications · 2025Article
- cGAS-STING targeting offers novel therapeutic regimen in sepsis-associated organ dysfunction.Cell biology and toxicology · 2025Review
- Review
- New developments in the role of ferroptosis in sepsis‑induced cardiomyopathy (Review).Molecular medicine reports · 2025Review
- Esketamine alleviated cardiomyocyte ferroptosis induced by oxygen-glucose deprivation/reoxygenation (OGD/R) via cyclic GMP-AMP synthase interactor.Cytotechnology · 2025Article
- Advances in neutrophil extracellular traps and ferroptosis in sepsis-induced cardiomyopathy.Frontiers in immunology · 2025Review
- MicroRNA-27b alleviates septic cardiomyopathy by targeting the Mff/MAVS axis.Frontiers in cellular and infection microbiology · 2025Article
- An emerging double‑edged sword role of ferroptosis in cardiovascular disease (Review).International journal of molecular medicine · 2025Review
- NLRP3 Inflammasome Targeting Offers a Novel Therapeutic Paradigm for Sepsis-Induced Myocardial Injury.Drug design, development and therapy · 2025Review
- Ferroptosis mechanisms and regulations in cardiovascular diseases in the past, present, and future.Cell biology and toxicology · 2024Review
- Ferroptosis, a Regulated Form of Cell Death, as a Target for the Development of Novel Drugs Preventing Ischemia/Reperfusion of Cardiac Injury, Cardiomyopathy and Stress-Induced Cardiac Injury.International journal of molecular sciences · 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
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Previous studies have demonstrated that cardiomyocyte apoptosis, ferroptosis, and inflammation participate in the progress of sepsis-induced cardiomyopathy (SIC). Although Islet cell autoantigen 69 (ICA69) is an imperative molecule that could regulate inflammation and immune response in numerous illnesses, its function in cardiovascular disease, particularly in SIC, is still elusive. We confirmed that LPS significantly enhanced the expression of ICA69 in wild-type (WT) mice, macrophages, and cardiomyocytes. The knockout of ICA69 in lipopolysaccharide(LPS)-induced mice markedly elevated survival ratio and heart function, while inhibiting cardiac muscle and serum inflammatory cytokines, reactive oxygen (ROS), and ferroptosis biomarkers. Mechanistically, increased expression of ICA69 triggered the production of STING, which further resulted in the production of intracellular lipid peroxidation, eventually triggering ferroptosis and heart injury. Intriguingly, ICA69 deficiency only reversed the ferroptotic marker levels, such as prostaglandin endoperoxide synthase 2 (PTGS2), malonaldehyde (MDA), 4-hydroxynonenal (4HNE), glutathione peroxidase 4 (GPX4), superoxide dismutase (SOD), iron and lipid ROS, but had no effects on the xCT-dependent manner. Additionally, greater ICA69 level was identified in septic patients peripheralblood mononuclear cells (PBMCs) than in normal control groups. Generally, we unveil that ICA69 deficiency can relieve inflammation and ferroptosis in LPS-induced murine hearts and macrophages, making targeting ICA69 in heart a potentially promising treatment method for SIC.
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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.