Janka Babickovas bilde

Janka Babickova

Forsker, Researcher
  • E-postjanka.babickova@uib.no
  • Besøksadresse
    Haukeland universitetssykehus, Laboratoriebygget
    5009 Bergen
  • Postadresse
    Postboks 7804
    5020 Bergen
Vitenskapelig artikkel
  • Vis forfatter(e) (2023). Proteomic analysis unveils Gb3-independent alterations and mitochondrial dysfunction in a gla <sup> −/−</sup> zebrafish model of Fabry disease. Journal of Translational Medicine.
  • Vis forfatter(e) (2023). Glomerular proteomic profiling reveals early differences between preexisting and de novo type 2 diabetes in human renal allografts. BMC Nephrology. 15 sider.
  • Vis forfatter(e) (2022). Six-week inhalation of lead oxide nanoparticles in mice affects antioxidant defense, immune response, kidneys, intestine and bones. Environmental Science: Nano. 751-766.
  • Vis forfatter(e) (2022). Reduced α-galactosidase A activity in zebrafish (Danio rerio) mirrors distinct features of Fabry nephropathy phenotype. Molecular Genetics and Metabolism Reports. 1-11.
  • Vis forfatter(e) (2022). Gene Expression Analysis in gla-Mutant Zebrafish Reveals Enhanced Ca<sup>2+</sup> Signaling Similar to Fabry Disease. International Journal of Molecular Sciences.
  • Vis forfatter(e) (2022). Extracellular DNA concentrations in various aetiologies of acute kidney injury. Scientific Reports. 11 sider.
  • Vis forfatter(e) (2022). Dynamics of Plasma and Urinary Extracellular DNA in Acute Kidney Injury. International Journal of Molecular Sciences. 1-8.
  • Vis forfatter(e) (2021). Ultrasound and Microbubbles Enhance Uptake of Doxorubicin in Murine Kidneys. Pharmaceutics.
  • Vis forfatter(e) (2021). The Effect of Melatonin on Periodontitis . International Journal of Molecular Sciences. 1-11.
  • Vis forfatter(e) (2021). Axl-inhibitor bemcentinib alleviates mitochondrial dysfunction in the unilateral ureter obstruction murine model. Journal of Cellular and Molecular Medicine. 7407-7417.
  • Vis forfatter(e) (2020). Plasma Concentrations of Extracellular DNA in Acute Kidney Injury. Diagnostics (Basel). 1-12.
  • Vis forfatter(e) (2020). Nuclear and Mitochondrial Circulating Cell-Free DNA Is Increased in Patients With Inflammatory Bowel Disease in Clinical Remission. Frontiers in medicine. 1-8.
  • Vis forfatter(e) (2020). A collagen-binding protein enables molecular imaging of kidney fibrosis in vivo. Kidney International. 609-614.
  • Vis forfatter(e) (2019). Six-week inhalation of CdO nanoparticles in mice: The effects on immune response, oxidative stress, antioxidative defense, fibrotic response, and bones. Food and Chemical Toxicology (FCT).
  • Vis forfatter(e) (2019). Oxidative Stress in Animal Models of Acute and Chronic Renal Failure. Disease Markers. 1-11.
  • Vis forfatter(e) (2019). AXL targeting reduces fibrosis development in experimental unilateral ureteral obstruction. Physiological Reports. 1-20.
  • Vis forfatter(e) (2018). Extracellular DNA as a prognostic and therapeutic target in mouse colitis under DNase I treatment. Folia biologica (Praha). 10-15.
  • Vis forfatter(e) (2018). Fabry nephropathy: Transcriptome sequencing of microdissected renal compartments from archival kidney biopsies at baseline, and after 5 & 10 years of enzyme replacement therapy.
Vitenskapelig oversiktsartikkel/review
  • Vis forfatter(e) (2024). Adverse effects of acute tubular injury on the glomerulus: contributing factors and mechanisms. Pediatric nephrology (Berlin, West).
  • Vis forfatter(e) (2020). Oxidative stress in the pathophysiology of kidney disease: Implications for noninvasive monitoring and identification of biomarkers. Oxidative Medicine and Cellular Longevity. 1-11.
  • Vis forfatter(e) (2018). Cell-free nucleic acids in urine as potential biomarkers of kidney disease. Journal of Applied Biomedicine. 157-164.
  • Vis forfatter(e) (2018). Cell-free DNA: the role in pathophysiology and as a biomarker in kidney diseases. Expert Reviews in Molecular Medicine. 1-14.

Se fullstendig oversikt over publikasjoner i CRIStin.


European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement (No. 842619-DIE_CKD).

About the project:

Chronic kidney disease (CKD) is a major cause of morbidity and mortality, affecting over 10 % of the adult population. Regardless of the primary case, the progressed stage is characterized by scarring of all anatomical elements of the kidney - glomeruli, tubulointerstitium, and vasculature referred to as renal fibrosis. Tubulointerstitial fibrosis has largely been viewed as a consequence of glomerular scarring, reflecting hypoxia downstream from the scarred glomeruli. Novel data suggest that ongoing communication between the glomerular and tubular compartments (tubuloglomerular feedback) plays an important role in the progression of renal fibrosis. Particularly, injury to the tubular compartments leads to more pronounced glomerular injury in the future. DIE_CKD is designed to uncover the range and mechanisms of tubular injuries involved in the pathogenic tubuloglomerular feedback. To achieve the project objectives, double/quadruple transgenic mice with the possibility of time-dependent, subsequent injury to different compartments of the kidney will be used. This unique approach will enable a direct study of how the injury to tubular compartments predisposes glomeruli to more severe injury. Detailed analysis of the mechanisms behind these effects will be performed. The experimental data will be further confirmed in human renal biopsies of patients with Fabry disease with progressed CKD and renal fibrosis. A comprehensive histopathological assessment of long-term prognosis of sequential biopsies will be performed to analyze the involvement of individual compartments over time.