ArticleBiochimica et biophysica acta. Molecular basis of disease2017
Mitochondrial dysfunction in rat splenocytes following hemorrhagic shock.
Article in Biochimica et biophysica acta. Molecular basis of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Therapeutic interventions to restore microcirculatory perfusion following experimental hemorrhagic shock and fluid resuscitation: A systematic review.Microcirculation (New York, N.Y. : 1994) · 2020Pooled it
- Modeling Hemorrhagic Shock in Male SD Rats by Fixed Volume Blood Withdrawal Followed by Partial Resuscitation and Long-Term Outcome Assessment.Medical sciences (Basel, Switzerland) · 2026Article
- Irisin deficiency exacerbates cardiac dysfunction and enhances hemorrhage injury in hemorrhage/resuscitation.American journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
- Hemorrhagic Shock and Mitochondria: Pathophysiology and Therapeutic Approaches.International journal of molecular sciences · 2025Review
- Phospholipase D regulates ferroptosis signal transduction in mouse spleen hypoxia response.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024Article
- BACH1-Hemoxygenase-1 axis regulates cellular energetics and survival following sepsis.Free radical biology & medicine · 2022Article
- Juvenile Plasma Factors Improve Organ Function and Survival following Injury by Promoting Antioxidant Response.Aging and disease · 2022Article
- Remote Ischemic Preconditioning Attenuates Hepatic Ischemia/Reperfusion Injury after Hemorrhagic Shock by Increasing Autophagy.International journal of medical sciences · 2021Article
- Protective Effect of Polydatin on Jejunal Mucosal Integrity, Redox Status, Inflammatory Response, and Mitochondrial Function in Intrauterine Growth-Retarded Weanling Piglets.Oxidative medicine and cellular longevity · 2020Article
- MicroRNA-34a (miR-34a) Mediates Retinal Endothelial Cell Premature Senescence through Mitochondrial Dysfunction and Loss of Antioxidant Activities.Antioxidants (Basel, Switzerland) · 2019Article
- Deficiency of metabolite sensing receptor HCA2 impairs the salutary effect of niacin in hemorrhagic shock.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
- NLRX1 Regulation Following Acute Mitochondrial Injury.Frontiers in immunology · 2019Article
- Anti-Hypoxic Molecular Mechanisms ofFrontiers in pharmacology · 2019Article
- A Combination Treatment Strategy for Hemorrhagic Shock in a Rat Model Modulates Autophagy.Frontiers in medicine · 2019Article
- Mesenteric lymph drainage alleviates hemorrhagic shock-induced spleen injury and inflammation.Acta cirurgica brasileira · 2019Article
- Kidney-targeted inhibition of protein kinase C-α ameliorates nephrotoxic nephritis with restoration of mitochondrial dysfunction.Kidney international · 2018Article
- Immune and metabolic alterations following trauma and sepsis - An overview.Biochimica et biophysica acta. Molecular basis of disease · 2017Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
The regulation of mitochondrial function is critical in cellular homeostasis following hemorrhagic shock. Hemorrhagic shock results in fluid loss and reduced availability of oxygen and nutrients to tissues. The spleen is a secondary lymphoid organ playing a key role in 'filtering the blood' and in the innate and adaptive immune responses. To understand the molecular basis of hemorrhagic shock, we investigated the changes in splenocyte mitochondrial respiration, and concomitant immune and metabolic alterations. The hemorrhagic injury (HI) in our rat model was induced by bleeding 60% of the total blood volume followed by resuscitation with Ringers lactate. Another group of animals was subjected to hemorrhage, but did not receive fluid resuscitation. Oxygen consumption rate of splenocytes were determined using a Seahorse analyzer. We found a significantly reduced oxygen consumption rate in splenocytes following HI compared to sham operated rats. The mitochondrial stress test revealed a decreased basal oxygen consumption rate, ATP production, maximal respiration and spare respiratory capacity. The mitochondrial membrane potential, and citrate synthase activity, were also reduced in the splenocytes following HI. Hypoxic response in the splenocyte was confirmed by increased gene expression of Hif1α. Elevated level of mitochondrial stress protein, hsp60 and induction of high mobility group box1 protein (HMGB1) were observed in splenocytes following HI. An increased inflammatory response was demonstrated by significantly increased expression of IL-6, IFN-β, Mip-1α, IL-10 and NFκbp65. In summary, we conclude that splenocyte oxidative phosphorylation and metabolism were severely compromised following HI.
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