ArticleJournal of bioenergetics and biomembranes2012
Endotoxemia impairs heart mitochondrial function by decreasing electron transfer, ATP synthesis and ATP content without affecting membrane potential.
Article in Journal of bioenergetics and biomembranes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 68 citations in OpenAlex.
- Reversible impairment of non-invasively assessed mitochondrial oxygen metabolism in the long-term course of patients with sepsis: a prospective monocentric cohort study.Intensive care medicine experimental · 2025Article
- Utility of melatonin on brain injury, synaptic transmission, and energy metabolism in rats with sepsis.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Mitochondria in health, disease, and aging.Physiological reviews · 2023Review
- Short-term Obesity Worsens Heart Inflammation and Disrupts Mitochondrial Biogenesis and Function in an Experimental Model of Endotoxemia.Inflammation · 2022Article
- Standardized fraction of Xylocarpus moluccensis inhibits inflammation by modulating MAPK-NFκB and ROS-HIF1α-PKM2 activation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Protective Effect of Mitochondria-Targeted Antioxidants against Inflammatory Response to Lipopolysaccharide Challenge: A Review.Pharmaceutics · 2021Review
- Mitochondrial Dynamics and VMP1-Related Selective Mitophagy in Experimental Acute Pancreatitis.Frontiers in cell and developmental biology · 2021Article
- The Metabolic Basis of Immune Dysfunction Following Sepsis and Trauma.Frontiers in immunology · 2020Review
- Mitochondrial bioenergetics links inflammation and cardiac contractility in endotoxemia.Basic research in cardiology · 2019Article
- Age-Dependent Myocardial Dysfunction in Critically Ill Patients: Role of Mitochondrial Dysfunction.International journal of molecular sciences · 2019Review
- Hemodynamic-Directed Cardiopulmonary Resuscitation Improves Neurologic Outcomes and Mitochondrial Function in the Heart and Brain.Critical care medicine · 2019Article
- Cellular Mechanisms of Myocardial Depression in Porcine Septic Shock.Frontiers in physiology · 2018Article
- Protective effects of exogenous NaHS against sepsis-induced myocardial mitochondrial injury by enhancing the PGC-1α/NRF2 pathway and mitochondrial biosynthesis in mice.American journal of translational research · 2018Article
- Mitochondrial-Targeted Antioxidant MitoQ PreventsJournal of lipids · 2018Article
- Deficiency of Soluble Epoxide Hydrolase Protects Cardiac Function Impaired by LPS-Induced Acute Inflammation.Frontiers in pharmacology · 2018Article
- Platelets and Multi-Organ Failure in Sepsis.International journal of molecular sciences · 2017Review
- Transcriptomic effects of adenosine 2A receptor deletion in healthy and endotoxemic murine myocardium.Purinergic signalling · 2017Article
- MITOCHONDRIAL FUNCTION IN SEPSIS.Shock (Augusta, Ga.) · 2016Review
- Oxidative-Nitrosative Stress and Myocardial Dysfunctions in Sepsis: Evidence from the Literature and Postmortem Observations.Mediators of inflammation · 2016Review
- Lipopolysaccharide Disrupts Mitochondrial Physiology in Skeletal Muscle via Disparate Effects on Sphingolipid Metabolism.Shock (Augusta, Ga.) · 2015Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute endotoxemia (LPS, 10 mg/kg ip, Sprague Dawley rats, 45 days old, 180 g) decreased the O₂ consumption of rat heart (1 mm³ tissue cubes) by 33% (from 4.69 to 3.11 μmol O₂/min. g tissue). Mitochondrial O₂ consumption and complex I activity were also decreased by 27% and 29%, respectively. Impaired respiration was associated to decreased ATP synthesis (from 417 to 168 nmol/min. mg protein) and ATP content (from 5.40 to 4.18 nmol ATP/mg protein), without affecting mitochondrial membrane potential. This scenario is accompanied by an increased production of O₂·⁻ and H₂O₂ due to complex I inhibition. The increased NO production, as shown by 38% increased mtNOS biochemical activity and 31% increased mtNOS functional activity, is expected to fuel an increased ONOO⁻ generation that is considered relevant in terms of the biochemical mechanism. Heart mitochondrial bioenergetic dysfunction with decreased O₂ uptake, ATP production and contents may indicate that preservation of mitochondrial function will prevent heart failure in endotoxemia.
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