ArticleOxidative medicine and cellular longevity2017
Oxidative Stress-Related Parthanatos of Circulating Mononuclear Leukocytes in Heart Failure.
Article in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 34 citations in OpenAlex.
- Article
- Lipid desaturation and cellular viability: mechanisms, stem cell insights, and a desaturation window model.Journal of lipid research · 2026Review
- The role of different types of programmed cell death in myocardial fibrosis: from mechanisms to therapeutics.Frontiers in cardiovascular medicine · 2026Review
- Programmed Cell Death in Heart Failure: Mechanisms, Impacts, and Therapeutic Prospects.Reviews in cardiovascular medicine · 2025Review
- The Role of Programmed Types of Cell Death in Pathogenesis of Heart Failure with Preserved Ejection Fraction.International journal of molecular sciences · 2024Review
- Hydrogen alleviates hypoxic-ischaemic brain damage in neonatal rats by inhibiting injury of brain pericytes.Journal of cellular and molecular medicine · 2024Article
- Deregulation of New Cell Death Mechanisms in Leukemia.Cancers · 2024Review
- Dexmedetomidine Inhibits Parthanatos in Cardiomyocytes and in Aortic Banded Mice by the ROS-Mediated NLRP3 Inflammasome Activation.Journal of cardiovascular translational research · 2023Article
- Molecular Mechanisms of Parthanatos and Its Role in Diverse Diseases.International journal of molecular sciences · 2022Review
- Chronic Hyperglycaemia Inhibits Tricarboxylic Acid Cycle in Rat Cardiomyoblasts Overexpressing Glucose Transporter Type 4.International journal of molecular sciences · 2022Article
- ROS-triggered endothelial cell death mechanisms: Focus on pyroptosis, parthanatos, and ferroptosis.Frontiers in immunology · 2022Review
- CaMKII in Regulation of Cell Death During Myocardial Reperfusion Injury.Frontiers in molecular biosciences · 2021Review
- Fundamental Mechanisms of the Cell Death Caused by Nitrosative Stress.Frontiers in cell and developmental biology · 2021Review
- Oxidative Stress and Antioxidant Treatments in Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2020Review
- Association between Proinflammatory Markers, Leukocyte-Endothelium Interactions, and Carotid Intima-Media Thickness in Type 2 Diabetes: Role of Glycemic Control.Journal of clinical medicine · 2020Article
- Peripheral Blood Mononuclear Cells and Platelets Mitochondrial Dysfunction, Oxidative Stress, and Circulating mtDNA in Cardiovascular Diseases.Journal of clinical medicine · 2020Review
- Protective effects of hydrogen‑rich saline against experimental diabetic peripheral neuropathy via activation of the mitochondrial ATP‑sensitive potassium channel channels in rats.Molecular medicine reports · 2020Article
- Distinct Types of Cell Death and the Implication in Diabetic Cardiomyopathy.Frontiers in pharmacology · 2020Review
- Programmed necrosis in cardiomyocytes: mitochondria, death receptors and beyond.British journal of pharmacology · 2019Review
- The molecular machinery of regulated cell death.Cell research · 2019Review
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe present study aims to examine the oxidative stress-related activation of poly(ADP-ribose) polymerase (PARP), a cause of parthanatos in circulating mononuclear leukocytes of patients with chronic heart failure (CHF), that was rarely investigated in the human setting yet.
methodsPatients with CHF (
resultsPlasma PRX, leukocyte HNE, NT, PARylation, and AIF translocation were significantly higher in the heart failure group. Pro-BNP levels in all study subjects showed a significant positive correlation to PRX, OSI, leukocyte HNE, NT, PARylation, and AIF translocation. Ejection fraction negatively correlated with the same parameters. Among HF patients, a positive correlation of pro-BNP with PRX, OSI, and PARylation was still present.
conclusionsMarkers of oxidative-nitrative stress, PARP activation, and AIF translocation in blood components showed correlation to reduced cardiac function and the clinical appearance of CHF. These results may reinforce the consideration of PARP inhibition as a potential therapeutic target in CHF.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.