ReviewJournal of bioenergetics and biomembranes2017
Phospholipids in mitochondrial dysfunction during hemorrhagic shock.
Review in Journal of bioenergetics and biomembranes, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Lacticaseibacillus paracasei SX52-B Isolated from Centenarians' feces: Genomic Analysis and Hypoglycemic Activity Evaluation.Probiotics and antimicrobial proteins · 2026Article
- Mitochondrial-Inflammatory Axis Dysregulation Triggers Disulfidptosis and the Multifaceted Protective Mechanism of Bisphenol A Following Spinal Cord Injury.Molecular neurobiology · 2026Article
- Biomarker Discovery in Childhood Asthma: A Pilot Study of Serum Metabolite Analysis for IgE-Dependent Allergy.Medical science monitor : international medical journal of experimental and clinical research · 2025Article
- Targeting mitochondrial quality control: new therapeutic strategies for major diseases.Military Medical Research · 2024Review
- Cerebrospinal fluid metabolite alterations in patients with different etiologies, diagnoses, and prognoses of disorders of consciousness.Brain and behavior · 2023Article
- Whole Blood Redox Potential Correlates With Progressive Accumulation of Oxygen Debt and Acts as A Marker of Resuscitation in A Swine Hemorrhagic Shock Model.Shock (Augusta, Ga.) · 2018Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Energy deficiency plays a key role in the development of irreversible shock conditions. Therefore, identifying mitochondrial functional disturbances during hemorrhagic shock should be considered a prospective direction for studying its pathogenesis. Phospholipid (PL)-dependent mechanisms of mitochondrial dysfunction in the brain (i.e., in the frontal lobes of the cerebral hemispheres and medulla oblongata) and liver, which, when damaged, leads to an encephalopathy, are examined in this review. These mechanisms show strong regional specificity. Analyzing the data presented in this review suggests that the basis for mitochondrial functional disturbances is cholinergic hyperactivation, accompanied by a choline deficiency and membrane phosphatidylcholine (PC) depletion. Stabilization of the PL composition in mitochondrial membranes using "empty" PC liposomes could be one of the most important methods for eliminating energy deficiency during massive blood loss.
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Registered trials
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