ArticleJuntendo Iji zasshi = Juntendo medical journal2024
Mitochondrial Damage in Sepsis.
Article in Juntendo Iji zasshi = Juntendo medical journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
What it found
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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
11 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mitochondrial dysfunction in sepsis: nutritional strategies for restoring bioenergetic homeostasis.Frontiers in cellular and infection microbiology · 2026Pooled it
- Inflammation-driven mitochondrial dysfunction and ROS accumulation orchestrate pulmonary fibrotic remodeling in sepsis.Redox biology · 2026Article
- Endotoxin-induced Ferroptosis-associated Leukocyte Injury and DAMP Release in Sepsis: AnJuntendo medical journal · 2026Article
- Autophagy-ferroptosis crosstalk in sepsis: metabolic pathways, redox injury, and host-directed antioxidant nanomedicine.Frontiers in immunology · 2026Review
- Impaired peripheral mononuclear cell metabolism in patients at risk of developing sepsis: A cohort study.Journal of critical care medicine (Universitatea de Medicina si Farmacie din Targu-Mures) · 2026Article
- Evaluating the Diagnostic Value and Molecular Mechanism of Energy Metabolism-Related Gene PEA15 in Sepsis.Journal of inflammation research · 2026Article
- Cell-free DNA in sepsis: from molecular insights to clinical management.Military Medical Research · 2025Review
- Heat stress-induced mitochondrial damage and its impact on leukocyte function.Journal of intensive care · 2025Review
- 3D-Printable Photothermal and Temperature-Controlled Polycaprolactone Scaffolds Incorporating Gold Plasmonic Blackbodies for Bone Tissue Engineering.ACS applied materials & interfaces · 2025Article
- Impact of hyper- and hypothermia on cellular and whole-body physiology.Journal of intensive care · 2025Review
- Autophagy and autophagic cell death in sepsis: friend or foe?Journal of intensive care · 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria not only generate adenosine triphosphate (ATP) and act as the powerhouse of the cell but also contribute to host defense by producing reactive oxygen species. Therefore, mitochondrial damage in sepsis directly results in a shortage of energy currency and dysregulation of the immune system. Other than those, mitochondrial damage results in the release of highly dangerous mitochondrial DNA, facilitating acidosis by modulating the metabolism and inducing programmed cell death, thereby facilitating disease progression in sepsis. Various forms of cell death are induced by mitochondrial damage. Aponecrosis is a secondary conversion from apoptosis to necrosis. Although apoptosis is initially intended, it cannot be completed due to ATP depletion from mitochondrial damage, ultimately leading to inflammatory necrosis. Besides such accidental cell death, programmed inflammation-inducing cell deaths such as necroptosis, ferroptosis, and pyroptosis are induced by mitochondrial damage in sepsis. Based on these findings, the regulation of mitochondrial damage holds promise for the development of new therapeutic approaches for sepsis.
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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.