Grażyna Nowak
assistant professor
Also affiliated: University of Georgia (1995); University of Arkansas Medical Center (2020)
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Grażyna Nowak's research focuses on the cellular and molecular mechanisms underlying kidney function and injury, with a particular emphasis on mitochondrial health and metabolic processes within renal proximal tubule cells. Her work has investigated how various factors, including oxidative stress, growth factors like EGF, and autocrine signaling pathways involving TGF-beta 1, impact cellular metabolism, proliferation, and viability.
Her publications detail the role of specific signaling pathways, such as the ERK1/2 pathway and protein kinase C-epsilon, in modulating mitochondrial function and active sodium transport following oxidant injury in renal cells. She has also explored the effects of compounds like all-trans-retinoic acid on protein kinase C and the genetic factors, such as the p21WAF1/CIP1 gene, that influence apoptosis in renal cells treated with chemotherapeutic agents like cisplatin. Studies have also extended to the impact of radiation on mitochondria in other organs, such as the rat heart.
Nowak leads a research group and has a scholarly record including 75 publications and over 1,100 citations, with an h-index of 20. She has recently been active in research, with her most recent publication in 2021. Her collaborators at the University of Arkansas for Medical Sciences include Olivia Speed, Jasna Vuk, and Judit Megyesi.
Metrics
- h-index: 20
- Publications: 39
- Citations: 1,088
Positions
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assistant professor publications 1995–2021University of Arkansas for Medical Sciences Institution web page
Selected Publications
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Microlearning activities improve student comprehension of difficult concepts and performance in a biochemistry course (2023)
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γ-Tocotrienol Protects against Mitochondrial Dysfunction, Energy Deficits, Morphological Damage, and Decreases in Renal Functions after Renal Ischemia (2021)
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Deletion of VDAC1 Hinders Recovery of Mitochondrial and Renal Functions After Acute Kidney Injury (2020)
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Protein kinase Cα mediates recovery of renal and mitochondrial functions following acute injury (2019)
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Protein Kinases and Regulation of Mitochondrial Function in Ischemia/Reperfusion Injury (2018)
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Protein kinase Cε targets respiratory chain and mitochondrial membrane potential but not F0F1‐ATPase in renal cells injured by oxidant (2018)
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Deletion of protein kinase C-ε attenuates mitochondrial dysfunction and ameliorates ischemic renal injury (2016)
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Protein Kinase C-α Interaction with F0F1-ATPase Promotes F0F1-ATPase Activity and Reduces Energy Deficits in Injured Renal Cells (2015)
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Radiation-Induced Alterations in Mitochondria of the Rat Heart (2014)
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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes (2013)
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Protein kinase C-α interaction with iHSP70 in mitochondria promotes recovery of mitochondrial function after injury in renal proximal tubular cells (2013)
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Assessment of Mitochondrial Functions and Cell Viability in Renal Cells Overexpressing Protein Kinase C Isozymes (2013)
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Protein kinase C-α activation promotes recovery of mitochondrial function and cell survival following oxidant injury in renal cells (2012)
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Protein kinase C-ε activation induces mitochondrial dysfunction and fragmentation in renal proximal tubules (2011)
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γ-Tocotrienol Protects against Mitochondrial Dysfunction and Renal Cell Death (2011)
Collaboration Network
Top Collaborators
- Activation of ERK1/2 pathway mediates oxidant-induced decreases in mitochondrial function in renal cells
- Protein kinase C-ϵ modulates mitochondrial function and active Na+transport after oxidant injury in renal cells
- Protein kinase C-ε activation induces mitochondrial dysfunction and fragmentation in renal proximal tubules
- γ-Tocotrienol Protects against Mitochondrial Dysfunction and Renal Cell Death
- Succinate Ameliorates Energy Deficits and Prevents Dysfunction of Complex I in Injured Renal Proximal Tubular Cells
Showing 5 of 10 shared publications
- Lack of a functional p21WAF1/CIP1gene accelerates caspase-independent apoptosis induced by cisplatin in renal cells
- Integrative effects of EGF on metabolism and proliferation in renal proximal tubular cells
- Autocrine production and TGF-beta 1-mediated effects on metabolism and viability in renal cells
- Transforming growth factor-β1 inhibits regeneration of renal proximal tubular cells after oxidant exposure
- Stress Response in a Leporine Renal Cell Model
- Deletion of VDAC1 Hinders Recovery of Mitochondrial and Renal Functions After Acute Kidney Injury
- Deletion of protein kinase C-ε attenuates mitochondrial dysfunction and ameliorates ischemic renal injury
- Protein kinase Cα mediates recovery of renal and mitochondrial functions following acute injury
- γ-Tocotrienol Protects against Mitochondrial Dysfunction, Energy Deficits, Morphological Damage, and Decreases in Renal Functions after Renal Ischemia
- Activation of ERK1/2 pathway mediates oxidant-induced decreases in mitochondrial function in renal cells
- Protein kinase C-ϵ modulates mitochondrial function and active Na+transport after oxidant injury in renal cells
- Succinate Ameliorates Energy Deficits and Prevents Dysfunction of Complex I in Injured Renal Proximal Tubular Cells
- Ascorbic Acid Promotes Recovery of Cellular Functions Following Toxicant-Induced Injury
- Collagen IV promotes repair of renal cell physiological functions after toxicant injury
- Renal Cell Regeneration Following Oxidant Exposure: Inhibition by TGF-β1and Stimulation by Ascorbic Acid
- Analysis of the Toxic Effects of Linoleic Acid, 12,13-cis-Epoxyoctadecenoic Acid, and 12,13-Dihydroxyoctadecenoic Acid in Rabbit Renal Cortical Mitochondria
- Linoleic acid epoxide promotes the maintenance of mitochondrial function and active Na+ transport following hypoxia
- Analysis of the Toxic Effects of Linoleic Acid, 12,13-cis-Epoxyoctadecenoic Acid, and 12,13-Dihydroxyoctadecenoic Acid in Rabbit Renal Cortical Mitochondria
- Linoleic acid epoxide promotes the maintenance of mitochondrial function and active Na+ transport following hypoxia
- Radiation-Induced Alterations in Mitochondria of the Rat Heart
- γ-Tocotrienol Protects against Mitochondrial Dysfunction and Renal Cell Death
- Activation of ERK1/2 pathway mediates oxidant-induced decreases in mitochondrial function in renal cells
- Protein kinase C-α inhibits the repair of oxidative phosphorylation afterS-(1,2-dichlorovinyl)- l -cysteine injury in renal cells
- Direct Interaction of All-trans-retinoic Acid with Protein Kinase C (PKC)
- Ascorbic Acid Promotes Recovery of Cellular Functions Following Toxicant-Induced Injury
- Akt activation improves oxidative phosphorylation in renal proximal tubular cells following nephrotoxicant injury
- Akt Activation Diminishes Nephrotoxicant‐Induced Mitochondrial Dysfunction and Necrosis in Renal Cells
- Protein kinase C-α interaction with iHSP70 in mitochondria promotes recovery of mitochondrial function after injury in renal proximal tubular cells
- Protein kinase C-α interaction with iHSP70 in mitochondria promotes recovery of mitochondrial function after injury in renal proximal tubular cells
- Radiation-Induced Alterations in Mitochondria of the Rat Heart
- Radiation-Induced Alterations in Mitochondria of the Rat Heart
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