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Kidney Pathophysiology Research Group

Tacrolimus Treatment Causes Kidney Damage

  • April 10, 2023
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Use of immunosuppressant calcineurin inhibitors (CNIs) is limited by irreversible kidney damage, hallmarked by renal fibrosis. CNIs directly damage many renal cell types. Given the diverse renal cell populations, additional targeted cell types and signaling mechanisms warrant further investigation. We hypothesized that fibroblasts contribute to CNI-induced renal fibrosis and propagate profibrotic effects via the transforming […]

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Kidney Pathophysiology Research Group

Zinc Supplementation: A Possible Offramp from the Road to End Stage Kidney Failure

  • March 1, 2023
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Ume, Adaku C.; Wenegieme, Tara-Yesomi; Adesina, Sherry E.; Williams, Clintoria R. Globally, over 103 million individuals are afflicted by CKD, a silent killer claiming the lives of 1.2 million people annually. CKD is characterized by five progressive stages, in which dialysis and kidney transplant are life-saving routes for patients with end stage kidney failure. While kidney damage impairs kidney function […]

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Kidney Pathophysiology Reseach Group

CnAα Inhibition Drives NFκB Activation Thereby Promoting Nox2-Mediated Oxidative Stress

  • April 27, 2021
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Aswathy M. Cheriyan, Adaku C. Ume, Cynthia E. Francis, Keyona N. King, Valerie A. Linck, Yun Bai, Hui Cai, Robert S. Hoover, Heping P. Ma, Jennifer L. Gooch, and Clintoria R. Williams Calcineurin inhibitors (CNIs) are vital immunosuppressive therapies in the management of inflammatory conditions. A long-term consequence is nephrotoxicity. In the kidneys, the primary, […]

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Kidney Pathophysiology Research Group

Calcineurin Inhibitors: a Double-Edged Sword

  • March 9, 2021
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Adaku C. Ume, Tara-Yesomi Wenegieme, and Clintoria R. Williams Recently, research has directed its interests into identifying molecular pathways implicated in calcineurin inhibitor (CNI)-induced renal fibrosis. An emerging body of studies investigating calcineurin (CnA) activity has identified distinct actions of two main ubiquitously expressed isoforms: CnAα and CnAβ. CNIs have the capacity to inhibit both […]

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Zinc Deficiency Promotes Kidney Damage

  • April 4, 2020
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NADPH oxidase-2 mediates zinc deficiency-induced oxidative stress and kidney damage. Mirandy S. Li, Sherry E. Adesina, Carl L. Ellis, Jennifer L. Gooch, Robert S. Hoover and Clintoria R. Williams Zn2+ deficiency (ZnD) is comorbid with chronic kidney disease and worsens kidney complications. Oxidative stress is implicated in the detrimental effects of ZnD. However, the sources […]

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Zinc Deficiency Plays a Role in High Blood Pressure

  • January 23, 2019
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Zinc Deficiency Induces Hypertension by Promoting Renal Na+ Reabsorption Clintoria R. Williams, Monisha Mistry, Aswathy M. Cheriyan, Jasmine M. Williams, Meagan K. Naraine, Carla L. Ellis, Rickta Mallick, Abinash C. Mistry, Jennifer L. Gooch, Benjamin Ko, Hui Cai and Robert S. Hoover Zn2+ deficiency (ZnD) is a common comorbidity of many chronic diseases. In these […]

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Zinc is Important for Insulin Secretion

  • January 2, 2019
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Extracellular ATP and zinc are co-secreted with insulin and activate multiple P2X purinergic receptor channels expressed by islet beta-cells to potentiate insulin secretion. Richards-Williams C1, Contreras JL, Berecek KH, Schwiebert EM It is well established that ATP is co-secreted with insulin and zinc from pancreatic beta-cells (beta-cells) in response to elevations in extracellular glucose concentration. […]

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