ArticleShock (Augusta, Ga.)2008
Exogenous cytochrome C restores myocardial cytochrome oxidase activity into the late phase of sepsis.
Article in Shock (Augusta, Ga.), 2008. 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
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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
21 citing papers in PubMed, 52 citations in OpenAlex.
- Diverse functions of cytochrome c in cell death and disease.Cell death and differentiation · 2024Review
- Circulating N-lactoyl-amino acids and N-formyl-methionine reflect mitochondrial dysfunction and predict mortality in septic shock.Metabolomics : Official journal of the Metabolomic Society · 2024Article
- Targeting the alternative oxidase (AOX) for human health and food security, a pharmaceutical and agrochemical target or a rescue mechanism?The Biochemical journal · 2022Review
- Review
- The Surviving Sepsis Campaign: Basic/Translational Science Research Priorities.Critical care medicine · 2020Article
- The surviving sepsis campaign: basic/translational science research priorities.Intensive care medicine experimental · 2020Article
- Age-Dependent Myocardial Dysfunction in Critically Ill Patients: Role of Mitochondrial Dysfunction.International journal of molecular sciences · 2019Review
- Mitochondrial quality control mechanisms as potential therapeutic targets in sepsis-induced multiple organ failure.Journal of molecular medicine (Berlin, Germany) · 2019Review
- Potential therapy strategy: targeting mitochondrial dysfunction in sepsis.Military Medical Research · 2018Review
- Time course of liver mitochondrial function and intrinsic changes in oxidative phosphorylation in a rat model of sepsis.Intensive care medicine experimental · 2018Article
- Inducing cell death in vitro in cancer cells by targeted delivery of cytochrome c via a transferrin conjugate.PloS one · 2018Article
- Mitochondria mediate cell membrane repair and contribute to Duchenne muscular dystrophy.Cell death and differentiation · 2017Article
- Sepsis-Induced Cardiomyopathy: Mechanisms and Treatments.Frontiers in immunology · 2017Review
- MITOCHONDRIAL FUNCTION IN SEPSIS.Shock (Augusta, Ga.) · 2016Review
- Energy crisis: the role of oxidative phosphorylation in acute inflammation and sepsis.Biochimica et biophysica acta · 2014Review
- Increased cytochrome c in rat cerebrospinal fluid after cardiac arrest and its effects on hypoxic neuronal survival.Resuscitation · 2012Article
- Mitochondrial dysfunction and biogenesis: do ICU patients die from mitochondrial failure?Annals of intensive care · 2011Article
- The multiple functions of cytochrome c and their regulation in life and death decisions of the mammalian cell: From respiration to apoptosis.Mitochondrion · 2011Review
- Peritoneal inflammation in pigs is associated with early mitochondrial dysfunction in liver and kidney.Inflammation · 2010Article
- Hypoxia-induced alteration of mitochondrial genes in cardiomyocytes: role of Bnip3 and Pdk1.Shock (Augusta, Ga.) · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Mitochondrial dysfunction is thought to play a role in the pathogenesis of a variety of disease states, including sepsis. An acquired defect in oxidative phosphorylation potentially causes sepsis-induced organ dysfunction. Cytochrome oxidase (CcOX), the terminal oxidase of the respiratory chain, is competitively inhibited early in sepsis and progresses, becoming noncompetitive during the late phase. We have previously demonstrated that exogenous cytochrome c can overcome myocardial CcOX competitive inhibition and improve cardiac function during murine sepsis at the 24-h point. Here, we evaluate the effect of exogenous cytochrome c on CcOX activity and survival in mice at the later time points. Exogenous cytochrome c (800 microg) or saline was intravenously injected 24 h after cecal ligation and puncture (CLP) or sham operation. Steady-state mitochondrial cytochrome c levels and heme c content increased significantly 48 h post-CLP and remained elevated at 72 h in cytochrome c-injected mice compared with saline injection. Cecal ligation and puncture inhibited CcOX at 48 h in saline-injected mice. However, cytochrome c injection abrogated this inhibition and restored CcOX kinetic activity to sham values at 48 h. Survival after CLP to 96 h after cytochrome c injection approached 50% compared with only 15% after saline injection. Thus, a single injection of exogenous cytochrome c 24 h post-CLP repletes mitochondrial substrate levels for up to 72 h, restores myocardial COX activity, and significantly improves survival.
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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.