Marta Oknińska

ORCID: 0000-0001-5893-5755
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About
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Research Areas
  • Cardiac electrophysiology and arrhythmias
  • Pulmonary Hypertension Research and Treatments
  • Cardiovascular Function and Risk Factors
  • Heart rate and cardiovascular health
  • Cardiovascular Effects of Exercise
  • Cardiac pacing and defibrillation studies
  • Ion channel regulation and function
  • Nitric Oxide and Endothelin Effects
  • Cardiac Ischemia and Reperfusion
  • Multiple Myeloma Research and Treatments
  • Iron Metabolism and Disorders
  • Erythropoietin and Anemia Treatment
  • Cardiomyopathy and Myosin Studies
  • Cardiac Arrhythmias and Treatments
  • Hemoglobinopathies and Related Disorders
  • Autophagy in Disease and Therapy
  • Heart Rate Variability and Autonomic Control
  • RNA modifications and cancer
  • Pharmacological Effects and Toxicity Studies
  • Cardiac Valve Diseases and Treatments
  • Anesthesia and Neurotoxicity Research
  • Peptidase Inhibition and Analysis
  • Cancer, Hypoxia, and Metabolism
  • Protein Degradation and Inhibitors
  • ECG Monitoring and Analysis

Postgraduate School of Molecular Medicine
2020-2025

Centrum Medyczne Kształcenia Podyplomowego
2023

Abstract Although many cardioprotective interventions have been shown to limit infarct size (IS), in preclinical animal studies of acute myocardial ischemia/reperfusion injury (IRI), their clinical translation patient benefit has largely disappointing. A major factor is the lack rigor and reproducibility studies. To address this, we established IMproving Preclinical Assessment Cardioprotective Therapies (IMPACT) small multisite infarction (AMI) network, with centralized randomization blinded...

10.1007/s00395-025-01102-3 article EN cc-by Basic Research in Cardiology 2025-03-12

Development of heart failure (HF) after myocardial infarction (MI) is responsible for premature death. Complex cellular and molecular mechanisms are involved in this process. A number studies have linked the epitranscriptomic RNA modification N6-methyladenosine (m6A) with HF, but it remains unknown how m6A affects risk developing HF MI. We addressed regulation its demethylase fat mass obesity-associated (FTO) MI their association HF. Using liquid chromatography coupled to spectrometry, we...

10.3390/cells11152271 article EN cc-by Cells 2022-07-22

Pulmonary hypertension (PH) initially results in compensatory right ventricular (RV) hypertrophy, but eventually RV failure. This transition is poorly understood, may be triggered by hypoxia. Measurements of oxygen tension (pO2) PH are lacking. We hypothesized that hypoxia occurs monocrotaline-induced rats and myo-inositol trispyrophosphate (ITPP), facilitating dissociation from hemoglobin, can relieve it. Rats received monocrotaline or saline (control) 24 days later echocardiograms,...

10.1038/s41598-021-97470-6 article EN cc-by Scientific Reports 2021-09-09

The impact of sex and age on the arrhythmic susceptibility within setting acute ischemia is masked by fact that coronary events result from artery disease appearing with much earlier among men than women.LAD ligation or sham operations were performed in rats both sexes at 3 24 months. An ECG was recorded continuously for 6 h after operation. number early late premature ventricular beats (PVBs), episodes tachycardia (VT) fibrillation (VF), heart rate, QRS, QT Tpeak-Tend duration analysed....

10.1016/j.biopha.2021.111983 article EN cc-by Biomedicine & Pharmacotherapy 2021-08-12

Abstract The incidence of life-threatening ventricular arrhythmias, the most common cause sudden cardiac death (SCD), depends largely on arrhythmic substrate that develops in myocardium during aging process. There is a large deficit comparative studies development this both sexes, with particular paucity females. To identify substrates arrhythmia, fibrosis, cardiomyocyte hypertrophy, mitochondrial density, oxidative stress, antioxidant defense and intracellular Ca 2+ signaling isolated...

10.1038/s41598-024-53803-9 article EN cc-by Scientific Reports 2024-02-11

Abstract Heart failure is a consequence of progression hypoxia‐dependent tissue damages. Therapeutic approaches to restore and/or protect the healthy cardiac have largely failed and remain major challenge regenerative medicine. The myo‐inositol trispyrophosphate (ITPP) modifier haemoglobin which enters red blood cells modifies properties, allowing for easier better delivery oxygen by blood. Here, we show that this treatment approach in an vivo model myocardial infarction (MI) results...

10.1111/jcmm.14909 article EN cc-by Journal of Cellular and Molecular Medicine 2020-01-19

Multiple myeloma (MM) is associated with increased cardiovascular morbidity and mortality, while MM therapies also result in adverse cardiac effects. Endothelial dysfunction impaired nitric oxide (NO) pathway their possible mediator.Since arginase expression, resulting the consumption of ʟ-arginine, precursor for NO synthesis, our aim was to test if cardiotoxicity mediated by therapeutic, bortezomib (a proteasome inhibitor), can be ameliorated an inhibitor through improved endothelial...

10.3390/cancers15072191 article EN Cancers 2023-04-06

Exacerbations of chronic heart failure (CHF) are often treated with catecholamines to provide short term inotropic support, but this strategy is associated long-term detrimental hemodynamic effects and increased ventricular arrhythmias (VA), possibly related rate (HR). We hypothesized that ivabradine may prevent adverse short-term dopamine treatment in CHF.

10.1016/j.biopha.2021.111250 article EN cc-by Biomedicine & Pharmacotherapy 2021-01-13

Abstract Ventricular arrhythmias are a major source of early mortality in acute myocardial infarction (MI) and remain therapeutic challenge. Thus we investigated effects ivabradine, presumably specific bradycardic agent versus metoprolol, β-blocker, at doses offering the same heart rate (HR) reduction, on ventricular non-reperfused MI rat. Immediately after induction single dose ivabradine/ metoprolol was given. ECG continuously recorded were analyzed. After 6 h epicardial monophasic action...

10.1038/s41598-020-71706-3 article EN cc-by Scientific Reports 2020-09-14

Iron deficiency has been implicated in the pathophysiology of heart failure and myocardial ischemia reperfusion injury. Moreover, reperfused seems to lose iron, thus even subjects with normal iron status could benefit from therapy. Impaired mitochondrial respiration energy starvation may be among possible consequences deficiency. So far no attempts have made treat acute coronary syndromes iron. Thus our aim was verify hypothesis that intravenous therapy given during an infarction will reduce...

10.1016/j.biopha.2021.111893 article EN cc-by Biomedicine & Pharmacotherapy 2021-07-06

Multiple myeloma (MM) remains an incurable malignancy of plasma cells despite constantly evolving therapeutic approaches including various types immunotherapy. Increased arginase activity has been associated with potent suppression T-cell immune responses in different cancer. Here, we investigated the role 1 (ARG1) Vκ*MYC model MM mice. ARG1 expression myeloid correlated tumor progression and was accompanied by a systemic drop ʟ-arginine levels. In MM-bearing mice antigen-induced...

10.1038/s41598-022-24137-1 article EN cc-by Scientific Reports 2022-11-16

Right ventricular dysfunction (RVD) can follow primary pulmonary diseases, but the most common cause of its development is left-sided heart failure (HF). RVD associated with HF progression, increased risk death and hospitalisation. The mechanism right ventricle (RV) remodelling leading to due not fully elucidated. Rats underwent LAD ligation induce extensive left (LV) myocardial infarction (MI) subsequent HF. Sham-operated animals served as controls. After 8 weeks follow-up, LV RV...

10.3390/biom12111714 article EN cc-by Biomolecules 2022-11-19

Abstract Background and Purpose Pulmonary hypertension (PH) results from pulmonary vasculopathy, initially leading to a compensatory right ventricular (RV) hypertrophy, eventually RV failure. Hypoxia can trigger both vasculopathy Therefore, we tested if myo‐inositol trispyrophosphate (ITPP), which facilitates oxygen dissociation haemoglobin, relieve hypoxia, prevent failure mortality in the rat model of monocrotaline‐induced PH. Experimental approach Rats were injected with monocrotaline or...

10.1111/bph.16482 article EN British Journal of Pharmacology 2024-07-01

Abstract Pulmonary arterial hypertension (PAH) initially results in compensatory RV hypertrophy, but eventually failure. This transition is poorly understood, may be triggered by hypoxia. Measurements of oxygen tension (pO 2 ) PAH are lacking. We hypothesized that hypoxia occurs monocrotaline-induced rats and myo-inositol trispyrophosphate (ITPP), facilitating dissociation from hemoglobin, can relieve it. Rats received monocrotaline or saline (control) 24 days later echocardiograms,...

10.21203/rs.3.rs-572950/v1 preprint EN cc-by Research Square (Research Square) 2021-06-03

Abstract Background The incidence of life-threatening ventricular arrhythmias, the most common cause sudden cardiac death (SCD), depends largely on arrhythmic substrate that develops in myocardium during aging process. There is a huge deficit comparative studies development this both sexes, with particular paucity females. Methods To identify arrhythmia, fibrosis, cardiomyocyte hypertrophy, mitochondrial density, level oxidative stress, antioxidant defense and intracellular Ca 2+ signaling...

10.21203/rs.3.rs-3161749/v1 preprint EN cc-by Research Square (Research Square) 2023-09-02

Background: Exacerbations of chronic heart failure (CHF) are often treated with catecholamines to provide short term inotropic support, but this strategy is associated long-term detrimental hemodynamic effects and increased ventricular arrhythmias (VA), possibly related rate (HR). We hypothesized that ivabradine may prevent adverse short-term dopamine treatment in CHF. Methods: Rats post-myocardial infarction CHF received 2-week infusion saline, dopamine(D), ivabradine(I) or D&I; cardiac...

10.2139/ssrn.3719063 article EN SSRN Electronic Journal 2020-01-01
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