ArticlePloS one2011
Modulation of myocardial mitochondrial mechanisms during severe polymicrobial sepsis in the rat.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 44 citations in OpenAlex.
- Multi-omics nominates VDAC2 as a candidate protective locus in sepsis-associated cholesterol dysregulation.Apoptosis : an international journal on programmed cell death · 2025Article
- Notoginsenoside R1 improves intestinal microvascular functioning in sepsis by targeting Drp1-mediated mitochondrial quality imbalance.Pharmaceutical biology · 2024Article
- Article
- PINK1 contained in huMSC-derived exosomes prevents cardiomyocyte mitochondrial calcium overload in sepsis via recovery of mitochondrial CaStem cell research & therapy · 2021Article
- Knockdown of VDAC1 alleviates the cognitive dysfunction secondary to sepsis-associated encephalopathy.American journal of translational research · 2021Article
- Mitochondrial Functions in Infection and Immunity.Trends in cell biology · 2020Review
- Potential therapy strategy: targeting mitochondrial dysfunction in sepsis.Military Medical Research · 2018Review
- Analysis on sarcoglycans expression as markers of septic cardiomyopathy in sepsis-related death.International journal of legal medicine · 2018Observational
- Association between 4-year all-cause mortality and carnitine profile in maintenance hemodialysis patients.PloS one · 2018Article
- High-density lipoprotein, mitochondrial dysfunction and cell survival mechanisms.Chemistry and physics of lipids · 2016Review
- Cerium oxide nanoparticles attenuate acute kidney injury induced by intra-abdominal infection in Sprague-Dawley rats.Journal of nanobiotechnology · 2015Article
- Mitochondrial Mechanisms in Septic Cardiomyopathy.International journal of molecular sciences · 2015Review
- Bioenergetic programming of macrophages by the apolipoprotein A-I mimetic peptide 4F.The Biochemical journal · 2015Article
- Ethyl pyruvate reduces hepatic mitochondrial swelling and dysfunction in a rat model of sepsis.International journal of clinical and experimental pathology · 2015Article
- Pathophysiology of the cardio-renal syndromes types 1-5: An uptodate.Indian heart journalReview
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundWe tested the hypothesis that 5-Hydroxydecanoic acid (5HD), a putative mitoK(ATP) channel blocker, will reverse sepsis-induced cardiodynamic and adult rat ventricular myocyte (ARVM) contractile dysfunction, restore mitochondrial membrane permeability alterations and improve survival. METHODOLOGY/PRINCIPAL
findingsMale Sprague-Dawley rats (350-400 g) were made septic using 400 mg/kg cecal inoculum, ip. Sham animals received 5% dextrose water, ip. The Voltage Dependent Anion Channels (VDAC1), Bax and cytochrome C levels were determined in isolated single ARVMs obtained from sham and septic rat heart. Mitochondria and cytosolic fractions were isolated from ARVMs treated with norepinephrine (NE, 10 µmoles) in the presence/absence of 5HD (100 µmoles). A continuous infusion of 5HD using an Alzet pump reversed sepsis-induced mortality when administered at the time of induction of sepsis (-40%) and at 6 hr post-sepsis (-20%). Electrocardiography revealed that 5HD reversed sepsis-induced decrease in the average ejection fraction, Simpsons+m Mode (53.5±2.5 in sepsis and 69.2±1.2 at 24 hr in sepsis+5HD vs. 79.9±1.5 basal group) and cardiac output (63.3±1.2 mL/min sepsis and 79.3±3.9 mL/min at 24 hr in sepsis+5HD vs. 85.8±1.5 mL/min basal group). The treatment of ARVMs with 5HD also reversed sepsis-induced depressed contractility in both the vehicle and NE-treated groups. Sepsis produced a significant downregulation of VDAC1, and upregulation of Bax levels, along with mitochondrial membrane potential collapse in ARVMs. Pretreatment of septic ARVMs with 5HD blocked a NE-induced decrease in the VDAC1 and release of cytochrome C.
conclusionThe data suggest that Bax activation is an upstream event that may precede the opening of the mitoK(ATP) channels in sepsis. We concluded that mitoK(ATP) channel inhibition via decreased mitochondrial membrane potential and reduced release of cytochrome C provided protection against sepsis-induced ARVM and myocardial contractile dysfunction.
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Registered trials
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