ArticleBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2021
Treprostinil reduces mitochondrial injury during rat renal ischemia-reperfusion injury.
Article in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Current perspectives and trends on the role of mitochondria in renal ischemia-reperfusion injury from 2005 to 2024: a bibliometric analysis and literature review.Frontiers in physiology · 2025Pooled it
- Survival and Hemodynamic Effects of Parenteral Prostanoids in High-Altitude Group 1 Pulmonary Hypertension: A Retrospective Cohort Study.Pulmonary medicine · 2026Article
- Identification of Biomarker in Kidney Stone Disease by Integrating Transcriptomics and Olink Proteomics: A Case-Control Study.Journal of inflammation research · 2026Article
- Long-Term Functional and Structural Renoprotection After Experimental Acute Kidney Injury in Subclinical Chronic Kidney Disease In Vivo.International journal of molecular sciences · 2025Article
- A cloud-based learning module for biomarker discovery.Briefings in bioinformatics · 2024Article
- Quantification of treprostinil concentration in rat and human using a novel validated and rapid liquid chromatography-tandem mass spectrometry method: Experimental and clinical applications in ischemia-reperfusion injury.Clinica chimica acta; international journal of clinical chemistry · 2024Article
- Comprehensive overview of the role of mitochondrial dysfunction in the pathogenesis of acute kidney ischemia-reperfusion injury: a narrative review.Journal of Yeungnam medical science · 2024Article
- Hepatic ischemia-reperfusion syndrome and its effect on the cardiovascular system: The role of treprostinil, a synthetic prostacyclin analog.World journal of gastrointestinal surgery · 2023Review
- Selenoprotein Gene mRNA Expression Evaluation During Renal Ischemia-Reperfusion Injury in Rats and Ebselen Intervention Effects.Biological trace element research · 2023Article
- GPX3 and GSTT1 as biomarkers related to oxidative stress during renal ischemia reperfusion injuries and their relationship with immune infiltration.Frontiers in immunology · 2023Article
- Roles of Mitochondrial DNA Damage in Kidney Diseases: A New Biomarker.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundRenal ischemia-reperfusion injury (IRI) is a major factor contributing to acute kidney injury and it is associated with a high morbidity and mortality if untreated. Renal IRI depletes cellular and tissue adenosine triphosphate (ATP), which compromises mitochondrial function, further exacerbating renal tubular injury. Currently, no treatment for IRI is available. This study investigates the protective role of treprostinil in improving mitochondria biogenesis and recovery during rat renal IRI.
methodsMale Sprague Dawley rats were randomly assigned to groups: control, sham, IRI-placebo or IRI-treprostinil and subjected to 45 min of bilateral renal ischemia followed by 1-72 h reperfusion. Placebo or treprostinil (100 ng/kg/min) was administered subcutaneously via an osmotic minipump.
resultsTreprostinil significantly reduced peak elevated serum creatinine (SCr) levels and accelerated normalization relative to IRI-placebo (p < 0.0001). Treatment with treprostinil also inhibited IRI-mediated renal apoptosis, mitochondrial oxidative injury (p < 0.05), and the release of cytochrome c (p < 0.01) vs. IRI-placebo. In addition, treprostinil preserved renal mitochondrial DNA copy number (p < 0.0001) and renal ATP levels (p < 0.05) to nearly those of sham-operated animals. Non-targeted semi-quantitative proteomics showed reduced levels of ATP synthase subunits in the IRI-placebo group which were restored to sham levels by treprostinil treatment (p < 0.05). Furthermore, treprostinil reduced renal IRI-induced upregulated Drp1 and pErk protein levels, and restored Sirt3 and Pgc-1α levels to baseline (p < 0.05).
conclusionsTreprostinil reduces mitochondrial-mediated renal apoptosis, inhibits mitochondria fission, and promotes mitochondria fusion, thereby accelerating mitochondrial recovery and protecting renal proximal tubules from renal IRI. These results support the clinical investigation of treprostinil as a viable therapy to reduce renal IRI.
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