Volker Hans Haase

Professor of Medicine, Cancer Biology and Molecular Physiology and Biophysics, The Krick-Brooks Chair in Nephrology

Vanderbilt University School of Medicine

United States

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Volker Hans Haase is a Professor of Medicine, specializing in Cancer Biology and Molecular Physiology and Biophysics, at Vanderbilt University School of Medicine in the United States. His research primarily focuses on hypoxia-inducible factors, mitochondrial metabolism, and renal anemia therapies. Recent publications highlight innovative treatments for chronic kidney disease and their underlying biological mechanisms. He holds the Krick-Brooks Chair in Nephrology, contributing significantly to the field of nephrology through his research and clinical expertise.

Articles (14)

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2024

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2022

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2021

Collaborators (2)

Talat Ikizler

Vanderbilt University Medical Center

UNITED STATES

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Yvonne Zuchowski

Vanderbilt University Medical Center

UNITED STATES

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Volker Hans Haase

Research Interests

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Articles (14)

Disruption of nucleotide biosynthesis reprograms mitochondrial metabolism to inhibit adipogenesis.

Disruption of mitochondrial electron transport impairs urinary concentration via AMPK-dependent suppression of aquaporin 2

Hypoxia-inducible factor activators: a novel class of oral drugs for the treatment of anemia of chronic kidney disease.

Novel Anemia Therapies in Chronic Kidney Disease: Conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference.

Lipid kinase PIK3C3 maintains healthy brown and white adipose tissues to prevent metabolic diseases

Updates on Hypoxia-Inducible Factor Prolyl Hydroxylase Inhibitors in the Treatment of Renal Anemia

Deregulating iron-erythropoiesis regulation: transferrin receptor 2 as potential target for treating anemia in CKD.

EPO synthesis induced by HIF‐PHD inhibition is dependent on myofibroblast transdifferentiation and colocalizes with non‐injured nephron segments in murine kidney fibrosis

Erythropoietic effects of vadadustat in patients with anemia associated with chronic kidney disease.

Inhibition of hypoxia-inducible factor-prolyl hydroxylation protects from cyclophosphamide-induced bladder injury and urinary dysfunction.

The ins and outs of ferric citrate

Disruption of mitochondrial complex III in cap mesenchyme but not in ureteric progenitors results in defective nephrogenesis associated with amino acid deficiency

Pharmacological HIF‐PHD inhibition reduces renovascular resistance and increases glomerular filtration by stimulating nitric oxide generation

Over-Generalizing About GC (Hypoxia): Pitfalls of Limiting Breadth of Experimental Systems and Analyses in Framing Informatics Conclusions

Collaborators (2)

Talat Ikizler

Yvonne Zuchowski

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